parasit4

Information about parasit4

Published on January 15, 2008

Author: Carla

Source: authorstream.com

Content

Malaria:  Malaria 1. Malaria is caused by several species of intracellular protozoan parasites of the genus Plasmodium. 2. The life cycle has many stages in humans (intermediate host) and Anopheles mosquito (definitive host). Start with the mosquito bite. Slide2:  d. The trophozoites grow without nuclear division to become mature trophozoites that fill much of the cell. e. The trophozoites then begin nuclear division and become schizonts. When nuclear division has produced 8 to 24 nuclei, cytoplasmic division takes place to yield mononucleate merozoites that are released to infect more red cells. Malaria- Schizonts:  Malaria- Schizonts Slide4:  f. Some merozoites enter red cells and (instead of making more merozoites) differentiate into macrogametocytes and microgametocytes, the precursors of the gametes. g. The gametocytes are taken up by a second mosquito with its blood meal. h. In the mosquito (the definitive host), the microgametocyte differentiate into flagellated male gametes (microgametes). The macrogametocyte becomes the female gametes (macrogamete). i. The male and female gametes fuse to form a zygote which matures into an ookinete, which becomes oocyst, which releases sporozoytes in the mosquito. Slide6:  3. Here are the essentials: Name of stage Comes from Infects Progeny become Sporozoite mosquito liver cells merozoites Merozoite liver cells or red cells merozoites or red cells (rarely) gametocytes Gametocyte red cells mosquito sporozoites (after a number of intermediate stages) Slide7:  4. Species of human malaria: a. Plasmodium falciparum b. Plasmodium vivax c. Plasmodium malariae d. Plasmodium ovale 5. The diagnostic stage is the various erythrocytic forms observed in blood smears. In most cases, the laboratory diagnosis of malaria is easy if you think of doing it. Thick and thin smears of blood should be prepared. Slide8:  6. The intrinsic incubation period (the incubation period in humans) is usually relatively short, 10-40 days. But it can be longer in P. vivax (6-12 months) because of a dormant stage in the liver. P. malariae may sometimes have an even longer incubation period of years or decades because of a chronic asymptomatic erythrocytic phase. Slide9:  7. Prodromal symptoms of headache, anorexia, fever, joint pains often lead to an initial false diagnosis of influenza in regions in which malaria is uncommon. The distinctive primary attack begins with a shaking chill of about an hour followed by a longer hot stage with headache and often nausea and vomiting. A heavy sweat ends this cycle, which eventually begins to recur with characteristic periodicity as the blood stages become synchronized. However, in the early days of disease, daily fever spikes are common. Anemia is caused by red blood cell destruction. Chronic reinfection in endemic areas results in splenomegaly. ALTERNATIVE PATHWAY FOR ACQUISISTION OF MALARIA:  ALTERNATIVE PATHWAY FOR ACQUISISTION OF MALARIA 1. All species of Plasmodium that infect humans can also be transmitted by blood transfusion. 2. All species of Plasmodium that infect humans can cause perinatal or transplacental infections of the newborn, but this pathway is rare. Slide14:  falciparum vivax malariae Average incub ~ 2 wks ~ 2 wks ~ 3 wks (or 6-12 mo) (or years) Fever periodicity 2 days 2 days 3 days Average parasitized 300.000 20.000 6.000 RBC/mm3 RBC preference any reticulocytes old RBC Relapse tendency low intermediate high Time before weeks months years relapse CHEMOTHERAPY OF MALARIA:  CHEMOTHERAPY OF MALARIA 1. Many drugs are available to inhibit growth of the erythrocytic stage. The CDC will supply current information on treatment. Some examples are: a. Chloroquine b. Pyremithamine plus sulfadoxine (Fansidar) c. Mefloquine Slide16:  2. Drug resistant parasites are a major problem. Chloroquine is useless against P. falciparum in most parts of the world. P. falciparum in some regions is resistant to most of the currently available drugs. (A very promising new drug is Artemisinin. No naturally occurring resistant strains have yet appeared). MALARIA PROPHYLAXIS:  MALARIA PROPHYLAXIS 1. Get up-to-date information. The recommendations are subject to change. Get up-to-date recommendations by calling the CDC. 2. The currently recommended malaria prophylaxis for areas in which chloroquine resistant P. falciparum is found is mefloquine. Slide18:  3. One drug, primaquine, is used primarily to eradicate the hypnozoite of P. vivax after a traveler returns home. 4. Bed nets (particularly those impregnated with insecticides) and insect repellents (DEET) applied to the skin are good protection against insect-born disease. HEMOFLAGELLATES :  HEMOFLAGELLATES 1. The remaining protozoa to be considered are called hemoflagellates because they are found in the blood at some stage in the life cycle and have flagella. Some species also have an obligate intracellular stage called the amastigote. All hemoflagellates have an insect host in their life cycle. It is not known which host (human or insect) is the definitive host. Slide20:  2. The flagellum of the hemoflagellates originates in an organelle (actually a mitochondrion) called the kinetoplast, which is rich in tiny circular DNA molecules and also contains the usual small circular mitochondrial genome. 3. Various stages of the parasite are identified on the basis of the localization of the kinetoplast and the flagellum. HEMOFLAGELLATES :  HEMOFLAGELLATES HEMOFLAGELLATES :  4. The hemoflagellates to be considered are a. African trypanosomes (African sleeping sickness). b. Various Leishmania species (various disease). c. Trypanosoma cruzy (Chagas’ disease) HEMOFLAGELLATES AFRICAN TRYPANOSOMIASIS:  AFRICAN TRYPANOSOMIASIS 1. African trypanosomiasis is caused by 2 species of an extracellular protozoan parasite. In contrast to the other hemoflagellates, the African trypanosomes are always extracellular. 2. The life cycle is relatively simple and requires the tsetse fly (genus glossina, several species). Slide26:  3. The diagnosis stage is the flagellated form in blood, lymph nodes biopsy, or CSF. 4. The 2 subspecies that cause African sleeping sickness differ in important characteristic, including a) time from infection to death (about 9 month vs years) b) role of other animals as alternative hosts vs exclusively human c) geographical focus (east vs west Africa) d) species of glossina (tsetse fly) Slide27:  5. A local nodule appears a few days after the bite of an infected fly 6. Two weeks after the bite: parasitemia, fever and lymphadenopathy (especially posterior cervival nodes- Wintterbottom’s sign). The parasites multiply in blood, lymph nodes and other tissues. Splenomegaly is common. 7. Invasion of the CSF with parasite multiplication in the CFS. 8. Lethargy, coma, and death. Slide28:  9. The names of the subspecies (for reference only) are Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense. 10. Treatment requires the use of highly toxic drugs, suramin for early (non CNS) infections and melarsoprol (an arsenical) for chronic CNS infections. 11. Severe disease caused by a related trypanosome in cattle has prevented the introduction of highly productive western breeds into large areas of Africa. The native ungulates are infected, but survive. Slide29:  12. Immunity is almost impossible to achieve, even after months of infection, because the blood-stage flagellates can change their major surface glycoprotein. Parasites with a different surface glycoprotein come to predominate as the immune response eliminates the one that preceded it. The end result is a sequence of waves of parasitemia and fever. The African trypanosomes have separate genes for hundreds of alternative surface antigens. A chromosomal rearrangement is often involved in shifting expression from one gene to another. 13. Prevention: avoid fly bites. LEISHMANIASIS:  LEISHMANIASIS 1. Leismaniasis is caused by several species of the protozoa genus Leishmania. They are predominantly intracellular parasites of the reticuloendothelial system. 2. The life cycle is simple: LEISHMANIASIS:  3. The diagnosis stage is the intracellular amastigote. It can be cultured (as extracellular form that is found in insects) as well as microscopically. 4. Treatment is difficult because the available drugs are toxic. Prevention requires avoidance of sand flies. LEISHMANIASIS Slide35:  5. The taxonomy of Leishmania is complex and you need to remember 2 groups: a. Visceral leishmaniasis caused by Leishmania donovani. b. Cutaneous or mucocutaneous leishmaniasis caused by various other Leishmania species. VISCERAL LEISHMANIASIS:  VISCERAL LEISHMANIASIS 1. Caused by Leishmania donovani in tropical Africa, Asia, and South America, temperate Asia, and focally in the Mediterranean basin. 2. Clinical picture: a. Incubation period 2-6 months or longer in some cases b. Insidious onset with fever (often twice a daily), enlarged spleen and lymph nodes, and hypergammaglobulinemia. c. Generally fatal if untreated Slide38:  3. Suspect kala-azar in patients with protracted fever (particularly non prostrating fever) and splenomegaly together with a suitable geographical history. 4. Diagnosis by marrow biopsy. The original cutaneous lesion is often healed before visceral symptoms appear, and few or no organisms can be found in the blood at that time. Slide39:  4. Diagnosis by marrow biopsy. The original cutaneous lesion is often healed before visceral symptoms appear, and few or no organisms can be found in the blood at that time. 5. Treatment with toxic antimony-containing drugs is mandatory. Amphitericin B is a promising treatment. CUTANEOUS LEISHMANIASIS:  CUTANEOUS LEISHMANIASIS 1. Caused by different Leishmania species in the Eastern and Western hemispheres. a. The “oriental sore” of Central Asia, India, Mediterranean basin, West Africa is usually seen on arms, legs, and face. b. The ulcer in the head is found in Central and South America. Slide41:  2. Clinical picture of cutaneous leishmaniasis: a. Incubation period 2-8 weeks b. Papule at site of bite slowly becomes 1-2 cm in diameter. c. Papule becomes an ulcer that lasts 6 months to several years. d. Scar and reasonably good immunity. Slide42:  3. Suspect cutaneous leishmaniasis in patients with an appropriate geographical history and chronic wet or dry ulcer. 4. Diagnosis by biopsy of the margin of a lesion. 5. The appropriate antimony drugs are toxic. If a lesion is not threatening a mucocutaneous junction, treatment can be delayed. Most cases are self-limiting and provide good immunity. Leishmaniasis in general:  Leishmaniasis in general 1. Treatment is the pentavalent antimony drug, sodium stibogluconate. 2. Prevention by avoiding sand flies. DTT controls the fly population very well. Chagas Disease:  Chagas Disease 1. Chagas’ disease is caused by Trypanosoma cruzi, a protozoan parasite with intracellular and extracellular stages. 2. The life cycle requires blood-sucking bugs (reduviid bugs). Slide47:  3. The diagnostic stage is the extracellular flagellated forms in the blood, but demonstration may be difficult in chronic disease. When seen the extracellular flagellated forms are often “C” shaped (for cruzi). 4. The initial infection is often mild or subclinical. Some persons have a painless swollen lesion near the eye at the site of the bite (Romaña’s sign). A few may die in the acute phase of infection (heart failure or meningitis). Slide48:  5. But 10% of serologically positive persons get chronic Chagas’ disease years or decades later. a. Myositis of cardiac muscle results in enlargement of the heart and congestive failure. b. Marked destruction of autonomic ganglia leads to mega-colon and mega-esophagus. c. About 3% of chronically infected pregnant women will have a transplacental infection of their fetuses. Slide51:  6. Diagnosis may be difficult, especially in the chronic form. In order of complexity: a. Look for flagellated form in blood smears (reliable only in the acute disease). b. Culture blood on blood agar for 3 months, looking for growth of the insect form. c. Inject mice with blood and look later for circulating flagellated form. Slide52:  6. d. Xenodiagnosis is the only reliable test in chronic disease. This test is not generally available. Feed laboratory-raised reduviid bugs on the patient, and check bug rectum for fecal parasites 1-2 months later. It may be replaced by PCR. e. A C-fixation test detects previous infection, but with poor sensitivity. Slide53:  7. The reduviid bugs live in substandard houses that provide crevices and cracks in the walls in which they must hide. When houses do not provide this shelter, they move to tree trunks and animal burrows. Thus, Chagas’ disease is more common in the poor. 8. Chagas’ disease is found only in South and Central America and in Mexico. Probably 12 million are chronically infected and at risk for chronic Chagas’ disease. Most of these would be positive in the xenodiagnostic test and can transmit Chagas’ disease by blood transfusion. Slide54:  9. Lampit is a toxic but reasonably effective drug for the acuter disease. The chronic disease is incurable. Surgery may be useful in mega-organ disease. 10. Prevention requires reduviid bug control and avoiding bug bites. Upgrading rural housing helps to reduce bug human contact. Summary:  Summary 1. Most of the world’s population is in developing nations, many of them in the tropics and subtropics. 2. In these nations, infectious diseases (many covered in this course), are the primary cause of disability and a major cause of death. 3. Although these nations seem far away, we have a responsibility to aid them in their struggle against infectious disease. Final Words:  Final Words “What seems to us more important, more painful and more unendurable is not really what is more important, more painful and more unendurable but merely that which is closest to home. Everything distant which for all its important moans and muffled cries, its ruined lives and millions of victims, that does not threaten to come rolling up to our threshold today we consider endurable and of tolerable dimensions.” -Alexander Solzhenitsyn, 1970, Nobel Prize Address Slide58:  “If in this world misery must exist, so be it; but let some little loophole, some glimpse of possibility at least, be left, which may serve the noble portion of humanity to hope and struggle unceasingly for its alleviation…” -Rabindranath Tagore, 1893

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