Blood
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BLOOD & TISSUE PROTOZOA I.
Toxoplasma gondii: A. Epidemiology: Worldwide distribution. Definitive host is the cat. 550% of people in various regions are seropositive. B. Mode of transmission: 1. 2. 3.
Contaminated food/water. Ingestion of raw or undercooked meat Transplacental infection.
C. Clinical manifestations: 1. 2. 3.
Immunocompetent host: Asymptomatic. Immunocompromised host: Reactivation disease. Congenital infection: Consequences depend upon the gestational age of the fetus. Spontaneous abortion, CNS damage, eye involvement. Only one-third of infected mothers give birth to infected infants of which 10% are symptomatic.
D. Pathology: Brain, lungs, liver, eyes are especially afffected (Toxoplasmic retinitis). Cell-mediated immunity is important in suppressing signs of infection. Containment in tissue cysts (bradyzoite form) is the normal outcome. Reactivation infection is typical in immunosuppressed patients, including HIV-positive or those maintained on immunosuppressive therapy (transplant recipients).
E. Laboratory diagnosis: Diagnosed by enzyme immunoassay for IgM antibody (acute) or IgG antibody (chronic). Banana-shaped trophs can be seen in Giemsa-stained blood smears during acute-phase infection from mice inoculated with patient samples (such as bronchoalveolar lavage fluid). Encysted bradyzoites can be observed in tissue biopsy material (lymph node). Calcified lesions may be apparent in X-ray films of brain. Toxoplasmamediated retinitis can be observed by opthalmoscopy. F. Treatment: No treatment in needed for healthy persons who are not pregnant. Symptoms will usually subside in a few weeks.
Combination of sulfadiazine and pyrimethamine for 3-4 weeks is recommended for pregnant woman with demonstrated acute infection and persons with weakened immune systems. II.
Plasmodium species: P. falciparum, P. vivax, P. malariae, P. ovale Over 200 million people affected worldwide. Nearly 1 million deaths/year. Humans are the intermediate host for Plasmodium; the mosquito is the definitive host. A. Epidemiology:
Occurs worldwide in the Tropics.
B. Mode of transmission: Zoonotic transmission viz female Anopheles mosquito, or (rarely) by inoculation of infected blood. C. Clinical manifestations: Abrupt onset fever (variable by of Plasmodium species). Symptoms also vary with the species but include chills, drenching sweats, anemia and splenomegaly. The fever pattern is typical of each species: Species P. vivax P. falciparum P. malariae P. ovale
Frequency Latency Fever Disease RBC of occurrence Period Pattern Severity Infection Most common 26 days Tertian Mild Retic’s Less common 12 days Tertian Severe All RBCs Least common 18-40 days Quartan Moderate Mature Rare 10-14 days Tertian Mild Retic’s
P. falciparum, P. vivax & P. ovale : tertian fever pattern = 48h (every third day). P. vivax & P. ovale produce latent infection in the liver (relapses). P. malariae: quartan fever pattern 72h (every 4th day). Falciparum malaria causes severe CNS manifestations and can be life-threatening (80%). Hemorrhage and necrosis can be associated. D. Pathology: Red blood cell destruction, both due to parasite lysis and splenic sequestering. Massive RBC lysis with Falciparum malaria (blackwater fever). Course of disease is more mild with other forms.
E. Laboratory diagnosis: Microscopic examination of Giemsa-stained blood smears. Gametocytes of P. falciparum are crescent-shaped; the others are sperical. F. Treatment:
4-aminoquinolines (Chloroquine, hydroxycholoroquine). 8-aminoquinoline (Primaquine). Quinine 1. Prophylaxis: Eliminates bloodstream forms before other cells are infected. Primaquine is the only drug that eliminates all forms. However, the therapy is problematic. 2. Suppressive theray: Inhibits early erythrocytic stage, circumvents clinical attack; Chloroquine treatment 1 week prior to arrival and 6 weeks after leaving from an endemic area (for P. falciparum, which is resistant, pyramethamine/sulfadoxine added with chloroquine). For P. ovale &/or P. vivax, primaquine added in weeks 5 & 6.
3. Clinical cure: Elimination of RBC forms to stop fever attacks. Most antimalarials will kill schizonts (exception is primaquine). Exoerythrocytic forms must continue to be suppressed. 4. Radical cure: Prevention of relapse by complete elimination. Includes 1 month of suppressive therapy to include primaquine for P. ovale and P. vivax infection.
III. Trypanosomes Species: T. cruzi (Chagas disease), T. gambiense & T. rhodesiense (African trypanosomiasis) Chagas disease A. Epidemiology: Central & South America. Vector-mediated transmission. B. Mode of transmission: Disease is initiated by the bite of the Triatoma (Reduviid bug). Humans & animals are both reservoir hosts (domestic and wild animals). Trypomastigotes are transferred to the arthropod vector during ingestion of a blood meal and can be transferred to a new human host. Tryps differentiate into nonflagellated amastigotes within mammalian host cells. Amastigotes differentiate back into trypomastigotes that enter the bloodstream to complete the cycle.
C. Pathology: 1.
Myocardial, glial and RES cells are most common intracellular growth sites. 2. Cardiac muscle is most severely affected. Neuronal damage gives rise to arrhythmias & loss of muscle tone in the colon & esophagus (megacolon & megaesophagus). 3. Acute phase: both tryps and amastigotes in the blood; Chronic phase: amastigotes in the tissues D. Clinical Considerations: Acute pahse = facial edema (related to site of bug bite) & “chagoma”. Fever lymphadenopathy & hepatosplenomegaly. Resolution in ~2 months. Chronic form may lead to death from cardiac arrhythmias & heart failure. May include autoimmune aspects. E. Laboratory diagnosis: Presence of tryps in thick or thin films. Stained biopsy specimens may reveal amastigotes. Xenodiagnosis involves infecting “clean” lab-raised reduviid bugs & demonstrating infection. Serology may be used. F. Treatment:
Nifurtimox kills tryps, but not amastigotes in tissues. No cure for chronic infection.
African trypanosomiasis (Sleeping sickness) A. Epidemiology: Endemic in sub-Saharan Africa. Vector transmission with a human reservoir for T. gambiense and domestic/wild animal reservoir for T. rhodesiense.
B. Mode of transmission: Tsetse fly (Glossina). Fly ingests tryps in blood meal, multiply in gut & migrate to salivary gland where they differentiate into amastigotes. Amastigotes differentiate into trypomastigotes after injection into mammalian host bloodstream. C. Pathology: 1.
Trypomastigotes spread from blood to lymph nodes and eventually to the brain. 2. Somnolence progresses to coma due to demyelinating encephalitis.
D. Clinical Considerations: Antigenic variation of trypomastigotes involves surface glycoproteins. This gives rise to an ability to evade host defenses & produce cyclic spiking fever in the acute phase. T. rhodesiense causes a more acute progressive disease. Trypanosoma gambiense disease is chronic and low-grade with progression to fatality over the course of a few years. E. Laboratory diagnosis: Blood smears, thick or thin film revealing trypomastigotes. Chancre or lymph node aspirates. CSF presence of trypomastigotes indicates encephalitic stage. Serology includes ELISA for IgM antibody to demonstrate acute infection. F. Treatment: Suramin is curative if given early enough. However, the drug does not pass blood-brain barrier. If CNS symptoms present, suramin with melarsoprol. Prevention includes avoiding bites (netting, sprays, protective clothing should be used in endemic areas). IV. Leishmaniasis Species include Leishmania donovani (kala-azar; visceral form), Leishmania tropica & Leishmania mexicana (cutaneous leishmaniasis), and Leishmania braziliensis (mucocutaneous leshmaniasis).
A. Epidemiology: Female sandfly vector (Phlebotomus, Old World; Lutzomyia, South America) and mammalian reservoir for Leishmania donovanii (dog, rodent); Mediteranean basin, Middle East, southern Russia and parts of China comprise one endemic region (dog & fox reservoir). Sub-Saharan Africa (civet & small carnivore reservoir) and India/Kenya (human reservior) are the other two.
B. Mode of transmission: The sandfly vector ingests macrophages containing the amastigotes. Amastigotes differentiate into flagellated promastigotes (occurs in the sandfly gut). Multiplication and migration to the pharynx and salivary glands makes the parasite available to infect a new host during subsequent blood meals (10 day cycle). In the human host, promastigotes are phagocytosed by macrophages & differentiate into amastigotes. Cells lyse & release amastigotes that infect other macrophages and RES cells.
C. Pathology: 1.
Visceral leishmaniasis includes infection of the liver, spleen and bone marrow (major organs of the RES). Anemia, leukopenia, & thrombocytopenia. 2. Cutaneous leishmaniasis: lesions are confined to the skin, with granuloma formation, ulceration and necrosis at the bite site (see picture below, on the far left). Initial papular lesion is called "Oriental Sore" or "Baghdad Boil", depending upon geography. 3. Mucocutaneous leishmaniasis: lesions occur on mucous membranes, cartilage and skin.
D. Clinical Considerations: Fever, weakness & weight loss. Massive splenic enlargement is characteristic. There is some skin hyperpigmentation in light-skinned patients. In cutaneous and mucocutaneous leishmaniasis the initial lesion is a papule with enlargement and satellite lesion formation, especially in the immunocompromised. The situation is similar to that seen in leprosy, with more profound nodular lesions in patients with decreased cellmediated immunity.
[Left to Right: Cutaneous lesion (closeup); Cutaneous Leishmaniasis; Mucocutaneous Form; Visceral Form (Kala-Azar)] E. Laboratory diagnosis: Detection of amastigotes in a bone marrow, spleen or lymph node biopsy for visceral; skin lesion smear for cutaneous/mucocutaneous. Serology using indirect IF. High IgG concentration is indicative. Leishmanin skin test can also be used (outside endemic area). F. Treatment: Sodium stibogluconate (pentavalent antimony). Mortality remains around 5% even with treatment. Recovered patients are immune to future infections. Prevention is by means of vector avoidance and insecticide use.
Toxoplasma gondii: A. Epidemiology: Worldwide distribution. Definitive host is the cat. 550% of people in various regions are seropositive. B. Mode of transmission: 1. 2. 3.
Contaminated food/water. Ingestion of raw or undercooked meat Transplacental infection.
C. Clinical manifestations: 1. 2. 3.
Immunocompetent host: Asymptomatic. Immunocompromised host: Reactivation disease. Congenital infection: Consequences depend upon the gestational age of the fetus. Spontaneous abortion, CNS damage, eye involvement. Only one-third of infected mothers give birth to infected infants of which 10% are symptomatic.
D. Pathology: Brain, lungs, liver, eyes are especially afffected (Toxoplasmic retinitis). Cell-mediated immunity is important in suppressing signs of infection. Containment in tissue cysts (bradyzoite form) is the normal outcome. Reactivation infection is typical in immunosuppressed patients, including HIV-positive or those maintained on immunosuppressive therapy (transplant recipients).
E. Laboratory diagnosis: Diagnosed by enzyme immunoassay for IgM antibody (acute) or IgG antibody (chronic). Banana-shaped trophs can be seen in Giemsa-stained blood smears during acute-phase infection from mice inoculated with patient samples (such as bronchoalveolar lavage fluid). Encysted bradyzoites can be observed in tissue biopsy material (lymph node). Calcified lesions may be apparent in X-ray films of brain. Toxoplasmamediated retinitis can be observed by opthalmoscopy. F. Treatment: No treatment in needed for healthy persons who are not pregnant. Symptoms will usually subside in a few weeks.
Combination of sulfadiazine and pyrimethamine for 3-4 weeks is recommended for pregnant woman with demonstrated acute infection and persons with weakened immune systems. II.
Plasmodium species: P. falciparum, P. vivax, P. malariae, P. ovale Over 200 million people affected worldwide. Nearly 1 million deaths/year. Humans are the intermediate host for Plasmodium; the mosquito is the definitive host. A. Epidemiology:
Occurs worldwide in the Tropics.
B. Mode of transmission: Zoonotic transmission viz female Anopheles mosquito, or (rarely) by inoculation of infected blood. C. Clinical manifestations: Abrupt onset fever (variable by of Plasmodium species). Symptoms also vary with the species but include chills, drenching sweats, anemia and splenomegaly. The fever pattern is typical of each species: Species P. vivax P. falciparum P. malariae P. ovale
Frequency Latency Fever Disease RBC of occurrence Period Pattern Severity Infection Most common 26 days Tertian Mild Retic’s Less common 12 days Tertian Severe All RBCs Least common 18-40 days Quartan Moderate Mature Rare 10-14 days Tertian Mild Retic’s
P. falciparum, P. vivax & P. ovale : tertian fever pattern = 48h (every third day). P. vivax & P. ovale produce latent infection in the liver (relapses). P. malariae: quartan fever pattern 72h (every 4th day). Falciparum malaria causes severe CNS manifestations and can be life-threatening (80%). Hemorrhage and necrosis can be associated. D. Pathology: Red blood cell destruction, both due to parasite lysis and splenic sequestering. Massive RBC lysis with Falciparum malaria (blackwater fever). Course of disease is more mild with other forms.
E. Laboratory diagnosis: Microscopic examination of Giemsa-stained blood smears. Gametocytes of P. falciparum are crescent-shaped; the others are sperical. F. Treatment:
4-aminoquinolines (Chloroquine, hydroxycholoroquine). 8-aminoquinoline (Primaquine). Quinine 1. Prophylaxis: Eliminates bloodstream forms before other cells are infected. Primaquine is the only drug that eliminates all forms. However, the therapy is problematic. 2. Suppressive theray: Inhibits early erythrocytic stage, circumvents clinical attack; Chloroquine treatment 1 week prior to arrival and 6 weeks after leaving from an endemic area (for P. falciparum, which is resistant, pyramethamine/sulfadoxine added with chloroquine). For P. ovale &/or P. vivax, primaquine added in weeks 5 & 6.
3. Clinical cure: Elimination of RBC forms to stop fever attacks. Most antimalarials will kill schizonts (exception is primaquine). Exoerythrocytic forms must continue to be suppressed. 4. Radical cure: Prevention of relapse by complete elimination. Includes 1 month of suppressive therapy to include primaquine for P. ovale and P. vivax infection.
III. Trypanosomes Species: T. cruzi (Chagas disease), T. gambiense & T. rhodesiense (African trypanosomiasis) Chagas disease A. Epidemiology: Central & South America. Vector-mediated transmission. B. Mode of transmission: Disease is initiated by the bite of the Triatoma (Reduviid bug). Humans & animals are both reservoir hosts (domestic and wild animals). Trypomastigotes are transferred to the arthropod vector during ingestion of a blood meal and can be transferred to a new human host. Tryps differentiate into nonflagellated amastigotes within mammalian host cells. Amastigotes differentiate back into trypomastigotes that enter the bloodstream to complete the cycle.
C. Pathology: 1.
Myocardial, glial and RES cells are most common intracellular growth sites. 2. Cardiac muscle is most severely affected. Neuronal damage gives rise to arrhythmias & loss of muscle tone in the colon & esophagus (megacolon & megaesophagus). 3. Acute phase: both tryps and amastigotes in the blood; Chronic phase: amastigotes in the tissues D. Clinical Considerations: Acute pahse = facial edema (related to site of bug bite) & “chagoma”. Fever lymphadenopathy & hepatosplenomegaly. Resolution in ~2 months. Chronic form may lead to death from cardiac arrhythmias & heart failure. May include autoimmune aspects. E. Laboratory diagnosis: Presence of tryps in thick or thin films. Stained biopsy specimens may reveal amastigotes. Xenodiagnosis involves infecting “clean” lab-raised reduviid bugs & demonstrating infection. Serology may be used. F. Treatment:
Nifurtimox kills tryps, but not amastigotes in tissues. No cure for chronic infection.
African trypanosomiasis (Sleeping sickness) A. Epidemiology: Endemic in sub-Saharan Africa. Vector transmission with a human reservoir for T. gambiense and domestic/wild animal reservoir for T. rhodesiense.
B. Mode of transmission: Tsetse fly (Glossina). Fly ingests tryps in blood meal, multiply in gut & migrate to salivary gland where they differentiate into amastigotes. Amastigotes differentiate into trypomastigotes after injection into mammalian host bloodstream. C. Pathology: 1.
Trypomastigotes spread from blood to lymph nodes and eventually to the brain. 2. Somnolence progresses to coma due to demyelinating encephalitis.
D. Clinical Considerations: Antigenic variation of trypomastigotes involves surface glycoproteins. This gives rise to an ability to evade host defenses & produce cyclic spiking fever in the acute phase. T. rhodesiense causes a more acute progressive disease. Trypanosoma gambiense disease is chronic and low-grade with progression to fatality over the course of a few years. E. Laboratory diagnosis: Blood smears, thick or thin film revealing trypomastigotes. Chancre or lymph node aspirates. CSF presence of trypomastigotes indicates encephalitic stage. Serology includes ELISA for IgM antibody to demonstrate acute infection. F. Treatment: Suramin is curative if given early enough. However, the drug does not pass blood-brain barrier. If CNS symptoms present, suramin with melarsoprol. Prevention includes avoiding bites (netting, sprays, protective clothing should be used in endemic areas). IV. Leishmaniasis Species include Leishmania donovani (kala-azar; visceral form), Leishmania tropica & Leishmania mexicana (cutaneous leishmaniasis), and Leishmania braziliensis (mucocutaneous leshmaniasis).
A. Epidemiology: Female sandfly vector (Phlebotomus, Old World; Lutzomyia, South America) and mammalian reservoir for Leishmania donovanii (dog, rodent); Mediteranean basin, Middle East, southern Russia and parts of China comprise one endemic region (dog & fox reservoir). Sub-Saharan Africa (civet & small carnivore reservoir) and India/Kenya (human reservior) are the other two.
B. Mode of transmission: The sandfly vector ingests macrophages containing the amastigotes. Amastigotes differentiate into flagellated promastigotes (occurs in the sandfly gut). Multiplication and migration to the pharynx and salivary glands makes the parasite available to infect a new host during subsequent blood meals (10 day cycle). In the human host, promastigotes are phagocytosed by macrophages & differentiate into amastigotes. Cells lyse & release amastigotes that infect other macrophages and RES cells.
C. Pathology: 1.
Visceral leishmaniasis includes infection of the liver, spleen and bone marrow (major organs of the RES). Anemia, leukopenia, & thrombocytopenia. 2. Cutaneous leishmaniasis: lesions are confined to the skin, with granuloma formation, ulceration and necrosis at the bite site (see picture below, on the far left). Initial papular lesion is called "Oriental Sore" or "Baghdad Boil", depending upon geography. 3. Mucocutaneous leishmaniasis: lesions occur on mucous membranes, cartilage and skin.
D. Clinical Considerations: Fever, weakness & weight loss. Massive splenic enlargement is characteristic. There is some skin hyperpigmentation in light-skinned patients. In cutaneous and mucocutaneous leishmaniasis the initial lesion is a papule with enlargement and satellite lesion formation, especially in the immunocompromised. The situation is similar to that seen in leprosy, with more profound nodular lesions in patients with decreased cellmediated immunity.
[Left to Right: Cutaneous lesion (closeup); Cutaneous Leishmaniasis; Mucocutaneous Form; Visceral Form (Kala-Azar)] E. Laboratory diagnosis: Detection of amastigotes in a bone marrow, spleen or lymph node biopsy for visceral; skin lesion smear for cutaneous/mucocutaneous. Serology using indirect IF. High IgG concentration is indicative. Leishmanin skin test can also be used (outside endemic area). F. Treatment: Sodium stibogluconate (pentavalent antimony). Mortality remains around 5% even with treatment. Recovered patients are immune to future infections. Prevention is by means of vector avoidance and insecticide use.
