Malaria is an infection with Plasmodium sp. Symptoms and signs include fever (possibly periodically), chills, sweating, hemolytic anemia and splenomegaly. The diagnosis is made by the optical detection of plasmodia in peripheral blood smears. Therapy and prophylaxis depend on the species and drug sensitivity; There are a fixed combination of atovaquone and proguanil, derivatives of artemisinin, doxycycline, mefloquine, chloroquine and quinine are available. With P. vivax or P. ovale infected patients also primaquine a recurrence get to prevent.
Malaria is Africa endemic in large areas of South and Southeast Asia, North and South Korea, Mexico, Central America, Haiti, the Dominican Republic, South America (including northern parts of Argentina), the Middle East (including Turkey, Syria, Iran and Iraq) and in Central Asia. The Centers for Disease Control and Prevention (CDC) have a maps app online that displays the most recent data on the prevalence of malaria worldwide; also included are the type of malaria, the resistance patterns and the recommended prophylaxis (s. CDC Malaria Map Application).
Malaria is an infection with Plasmodium sp. Symptoms and signs include fever (possibly periodically), chills, sweating, hemolytic anemia and splenomegaly. The diagnosis is made by the optical detection of plasmodia in peripheral blood smears. Therapy and prophylaxis depend on the species and drug sensitivity; There are a fixed combination of atovaquone and proguanil, derivatives of artemisinin, doxycycline, mefloquine, chloroquine and quinine are available. With P. vivax or P. ovale infected patients also primaquine a recurrence get to prevent. Malaria is Africa endemic in large areas of South and Southeast Asia, North and South Korea, Mexico, Central America, Haiti, the Dominican Republic, South America (including northern parts of Argentina), the Middle East (including Turkey, Syria, Iran and Iraq) and in Central Asia. The Centers for Disease Control and Prevention (CDC) have a maps app online that displays the most recent data on the prevalence of malaria worldwide; also included are the type of malaria, the resistance patterns and the recommended prophylaxis (s. CDC Malaria Map Application). between 300 and 500 million people worldwide are infected and it comes every year to about 655,000 deaths, mostly in children <5 years in Africa. Malaria occurred once also endemic in the United States. In the US, about 1,500 cases annually. Nearly all were purchased abroad, but very few come into being through blood transfusions or rarely through transfers by local mosquitoes after a blood meal of infected immigrants. Pathophysiology Plasmodium species that infect humans are P. falciparum P. vivax P. ovale P. malariae P. knowlesi A simultaneous infection with more than one Plasmodium species is unusual. Also transmissions from only occurring in other primates malaria variants ( "Simian Malaria") has been reported to humans; P. knowlesi is an emerging pathogen in Southeast Asia. The extent to which P. knowlesi is transmitted from person to person via mosquitoes without the monkeys as a natural intermediate host, is currently under investigation. The basic life cycle for all four Plasmodium sp. (Life cycle of Plasmodium.) Are identical. The cycle begins in that a female Anopheles mosquito a person suffering from malaria stings and sucks gametozytenhaltiges blood. During the next 1-2 weeks, the gametocytes multiply inside the mosquito sexually and form infectious sporozoites. When the mosquito bites another human, sporozoites are inoculated and reach the liver and infect hepatocytes. The parasites mature within the hepatocytes to Gewebeschizonten. Each schizont forms 10,000-30,000 merozoites that are released 1-3 weeks later in the rupture of the hepatocytes into the blood stream. Each merozoite can affect one red blood cells and be converted there into a trophozoite. The trophozoites grow and develop into erythrocyte schizonts. Schizonts form more merozoites, which leave the red blood cells rupture 48-72 hours later and released into the plasma. These merozoites then attacked quickly new red blood cells, and the cycle repeats itself. Some trophozoites develop into gametocytes, which are incorporated by Anopheles mosquito. They unite sexually in the gut of the mosquito, develop into oocysts and release infectious sporozoites which migrate to the salivary glands. Life cycle of Plasmodium. The life cycle of malaria parasites include two hosts. During a blood meal inoculated a malaria infected female Anopheles mosquito sporozoites into the human organism. Sporozoites infect the liver cells. There, the sporozoites mature into schizonts. The schizonts rupture and merozoites set free. This initial replication in the liver is called exoerythrozytischer cycle. Merozoites infect red blood cells. There, the parasite asexual (the so-called red cell cycle) increased. The merozoites develop into "ring shape" -Trophozoiten. Some then mature into schizonts. The schizonts rupture and merozoites set free. Some trophozoites differentiate into gametocytes. During a blood meal, an Anopheles mosquito swallows the male (Mikrogametozytes) and female (macrogametocytes) gametocytes and starts the sporogonen cycle. In the stomach of the mosquito, the microgamete penetrate the macrogametes and produce zygotes. The zygotes are movable and elongated and develop into ookinetes. The ookinetes penetrate the wall of the midgut of the mosquito, where they develop into oocysts. The oocysts grow, rupture and release sporozoites, which migrate to the salivary glands of the mosquito. Inoculation of the sporozoites into a new human host maintains the malaria life cycle. In P. vivax and P. ovale (but not P. falciparum or P. malariae), Gewebeschizonten may persist as Hypnozoiten in the liver for years. There are relapses of P. ovale after up to six years after an episode of symptomatic malaria occurred and the infection was transmitted through blood transfusion from a person who was exposed to seven years prior to blood donation. These dormant forms serve as "time bombs" that lead to relapses and may complicate chemotherapy because they are not killed by most drugs commonly used in circulating in the blood parasites are effective. The präerythrozytäre (hepatic) stage of the malaria life cycle is skipped if the infection is transmitted through blood transfusion, through the sharing of needles or congenital. Hence it is not a latent disease and delayed relapses in these types of transmission. The clinical symptoms associated with the rupture of red blood cells and thereby released merozoites. In a severe infection occurs due to the hemolysis to anemia and jaundice, which are exacerbated by the phagocytosis of infected erythrocytes in the spleen. In a P. falciparum - or chronic infection P. vivax can cause severe anemia, with P. malariae this is milder pronounced. Falciparum malaria (falciparum malaria) Unlike the other forms of malaria falciparum it comes to microvascular obstruction in P., as infected erythrocytes adhere to vascular endothelial cells. Because of ischemia tissue hypoxia arise in particular in the brain, kidneys, lungs and gastrointestinal tract. Hypoglycemia and lactic acidosis are other possible Komplikationen.Resistenz against infection Most West Africans have a complete resistance to P. vivax because their RBCs lack the Duffy blood group, which is required for the recognition of P. vivax in erythrocytes; many African Americans are resistant. The development of Plasmodium in red blood cells is delayed in patients with hemoglobin S, hemoglobin C, thalassemia, G6PD deficiency or elliptocytosis. Earlier infections result in partial immunity. If residents hyper endemic areas leave this goes acquired immunity back (months to years) and can occur when re-entry after infection to symptomatic malaria. Symptoms and signs The incubation period for P. vivax usually 12 to 17 days for P. falciparum usually 9-14 days, 16-18 days longer for P. ovale and about one month (18-40 days) or longer (years ) for P. malariae. However, some P. vivax strains temperate climates can lead to clinical disease takes months to> 1 year after infection. Manifestations that are common to all forms of malaria fever and chills – the paroxysmal attack of malaria anemia jaundice splenomegaly hepatomegaly The paroxysmal attack of malaria coincides with the release of merozoites from ruptured red blood cells along the classic bout of malaria begins with malaise, abrupt chills and fever, which on 39-41 ° C increases rapidly and filamentary pulse, polyuria, headache, myalgia and nausea. After 2-6 hours the fever drops again, and occurs within 2-3 h to heavy sweating, followed by extreme fatigue. The fever often rises at the beginning of the infection rapidly. For established development cycles malaria attacks mostly come depending on the species every 2-3 days before; However, the intervals are not rigid. Most splenomegaly is palpable at the end of the first clinical disease week, can falciparum in P. also missing. The enlarged spleen is soft and vulnerable to a traumatic rupture. With repeated recurrences of malaria splenomegaly may be declining due to the development of a functional immunity. After many attacks the spleen can fibrose be hard or in some patients massively enlarge (tropical splenomegaly). Usually it is also used in splenomegaly in a concomitant hepatomegaly. P. falciparum causes due to its microvascular effects of the most severe forms of the disease. It is the only Plasmodienart that with high probability, result in the absence of treatment to death; non-immune patients can die within days of their initial symptoms. Patients with cerebral malaria may develop symptoms ranging from an irritability of convulsions to coma. It may (a afebrile, shock-like syndrome) and lead to severe thrombocytopenia also lead to acute respiratory distress syndrome (ARDS), diarrhea, jaundice, epigastric discomfort, Netzhauthämorrhagien, algider malaria. Due to the volume depletion to renal insufficiency may develop by parasitically infected erythrocytes or deposition of immune complexes can cause vascular occlusion. Due to intravascular hemolysis haemoglobinemia hemoglobinuria and can result, which can be either (so named after the blackening of urine) spontaneously or after treatment with quinine in a blackwater fever proceed. Hypoglycaemia occurs frequently and can be enhanced by quinine associated with hyperinsulinemia. Placental contribution may lead to low birth weight, spontaneous abortion, stillbirth or a congenital infection. P. vivax, P. ovale and P. malariae usually not impair other organs. It rarely comes to deaths that come mostly through a ruptured spleen or uncontrolled Hyperparasitämie at asplenischen patients about. The clinical course of P. ovale is similar to that of P. vivax. For established infections temperature peaks in 48-h intervals occur on three-day pattern. P. malariae infections often do not cause acute symptoms, but a weak distinctive parasitaemia may persist for decades and lead to immune complex-mediated nephritis or nephrosis or tropical splenomegaly; at a symptomatic course of the fever tends in 72-h intervals to act-a four-day pattern. Malaria can (see table: prevention of malaria) in patients who have taken chemoprophylaxis, have an atypical. The incubation period can extend up to several months after you stop taking it for weeks. Infected individuals may develop headaches, back pain and irregular fever, but the parasite may initially be difficult to find in blood samples. Diagnostic light microscopy of blood (thin and thick smears) Rapid blood assays that detect Plasmodium antigens or enzymes fever and chills that occur when an immigrant or traveler coming from an endemic area should be cause for immediate investigation on malaria , Most cases occur within the first 6 months, but it can also take up to 2 years, rarely longer. A malaria can be diagnosed by the microscopic identification of parasites in the blood smear or thicknesses drops. The infecting species (which treatment and prognosis determined) is carried in the blood smear characteristics identified (see Table: diagnostic features for the differentiation of Plasmodium species in a blood smear). If the initial blood smear is negative, should be performed every 4-6 hours more blood smears. Thin blood smears stained with Wright-Giemsa stain allow an assessment of the morphology of the parasite within the erythrocyte, often speciation, and the determination of Parasitämieanteils. Thick blood smears are more sensitive, but more difficult to produce and evaluate, as the red blood cells are lysed prior to staining. Sensitivity and accuracy of the results depend on the experience of the examiner. Commercial rapid test based on the presence of certain Plasmodiumantigene or enzyme activities. Assays may be a histidine-rich protein 2 (HRP-2), the malaria parasites (in particular P. falciparum and P. vivax) is associated and plasmodiumassoziierte lactate dehydrogenase (pLDH) detected. The rapid tests are comparable in sensitivity in detecting low levels of parasitemia with microscopy; However, they do not distinguish a single infection of a simultaneous infection with more than one Plasmodium sp or leave a speciation to (with the exception of P. falciparum). Light microscopy and rapid tests are complementary examinations and both should be performed when they are available. They have a similar sensitivity. Negative results in both include malaria in a patient with low parasitaemia not. PCR and species-specific DNA probes can be used, but are not widely available. Because serological tests may indicate previous exposure, they are not suitable for the diagnosis of acute malaria. Diagnostic features for differentiation of Plasmodium species in the blood smear characteristic Plasmodium Vivax Falciparum Sp * malariae Enlarged infected erythrocytes Yes No No Schiiffner dots Yes No No Maurer’sche Fleckung or columns No Ja§ No Multiple infections in the erythrocytes Rarely Yes No ring molds with 2 Chromatinpunkten Rarely Frequently No crescent-shaped gametocytes No Yes No Bayonet or Bandtrophozoiten No No Yes schizonts in peripheral blood Yes Yes Rare number of merozoites per schizont (mean [Range]) 16 (12-24) 12 (8-24) ¶ 8 (6-12) * erythrocytes with P . oval are infected (fimbriae) are provided with fringes, oval and slightly larger; otherwise the parasite P. vivax are similar. P. knowlesi resembles morphologically P. malaria and was confused with either. A Schiiffner dots is best seen when the blood smear with Giemsa stain is colored. §Dieses feature is not always visible. ¶Schizonten are included in intestines and not usually present in the peripheral blood. Treatment antimalarials antimalarials are selected based on the clinical manifestations of the infecting Plasmodium sp, known resistance patterns of the tribes in the region of infection and the effectiveness and the side effects of available drugs. In some endemic areas, a considerable proportion of antimalarial drugs available on site is fake. That’s why some doctors advise travelers in remote areas with a high risk to take a full course of an appropriate treatment regimen used when a medically confirmed malaria is acquired despite prophylaxis; This strategy also avoids using up limited resources medicines in the target country. Malaria is particularly dangerous for children <5 years and pregnant women not previously exposed Visitors endemic areas. Mortality is highest among children <2 years. On suspicion of P. falciparum immediate therapy should be initiated, even if the initial smear is negative. P. falciparum and P. vivax, more recently, increasingly have resistances on to drugs against malaria. On recommended drugs and doses for the treatment and prevention of malaria, see table: treatment of malaria and prevention of malaria. Common side effects and contraindications are listed in side effects and contraindications of drugs against malaria. See the CDC website (Malaria Diagnosis and Treatment in the United States) or call for treatment advice whose Malaria Hotline at 770-488-7788 to (outside of business hours, on weekends or holidays, call 770-488-7100 to) , If there is a febrile illness while traveling in an endemic area, medical help should be sought immediately. If no quick evaluation is possible (for. Example, because the region is very remote), a self-medication with artemether / lumefantrine or atovaquone / proguanil can be done to the exclusion of malaria disease. If imagine travelers after returning from an endemic area with a fever and no other diagnosis is made, clinicians should consider for uncomplicated malaria the gift of an empirical treatment should, even if Malariaausstriche and / or rapid diagnostic tests are negative. Treatment of malaria preferences Medikamenta adult dosage dosage for Kinderb P. falciparum or unidentified species that have been acquired in all malaria areas, except those specified as chloroquine-sensitive are-oral medications. Drug of choice 4 certain adult tablets 1 times daily for 3 days <5 kg atovaquone / Proguanilc: Not Specified 5-8 kg: 2 for children 9-10 kg for 3 days certain tablets 1 time daily: 3 intended for children tablets 1 times daily for 3 days from 11 to 20 kg: 1 adult tablet intended for one-times daily for 3 days from 21 to 30 kg: 2 tablets intended for adults 1 times daily for 3 days from 31 to 40 kg: 3 for adults certain tablets 1 times daily for 3 days> 40 kg: 4 tablets intended for adults 1 times daily for 3 days or artemether / lumefantrind 6 doses (1 dose = 4 tablets) for 3 days (after 0 , 8, 24, 36, 48 and 60 h) 6 doses at intervals as for the adult; Dose = 5 <15 kg: 1 tablet 15- <25 kg: 2 tablets 25- <35 kg: 3 tablets ? 35 kg: 4 tablets or quinine sulfate plus one of the following: 650 mg all 8 h for 3 or 7 Tagee 10 mg / kg every 8 h for 3 or 7 Tagee Doxycyclinf 100 mg 2 times a day for 7 days 2.2 mg / kg 2 times daily for 7 days Tetracyclinf 250 mg 4 times daily for 7 days 6.25 mg / kg four times daily for 7 days Clindamycing 7 mg / kg 3 times daily for 7 days 7 mg / kg 3 times daily for 7 days Alternative (if no other options can be used) Mefloquinh 750 mg salt , then 500 mg salt 6-12 h later, 15 mg salt / kg, then 10 mg salt / kg 6-12 h later P. falciparum and unidentified species that were acquired in chloroquine-sensitive regions (Central America west of the Panama canal malariae, Haiti, Dominican Republic, the majority of the Middle East) and P. and P. knowl esi in all regions-oral drug agent of choice Chloroquinphosphati, j 1 g of salt (600 mg base), then 500 mg of salt (300 mg base) after 6, 24 and 48 h 10 mg / kg body weight (up to 600 mg base) then 5 mg base / kg after 6, 24 and 48 h or Hydroxychloroquinj 800 mg salt (620 mg base), then 400 mg of salt (310 mg base) after 6, 24 and 48 h 10 mg base / kg, then 5 mg / kg after 6, 24 and 48 h P. vivax (unless of chloroquine-resistant regions) or P. ovale oral medications drugs of choice Chloroquinphosphati, j or Hydroxychloroquinj dosed as above plus 30 mg Primaquink Base 1 times a day for 14 days 1 kg twice daily for 14 days P. vivax acquired in areas 0.5 mg base /, known -orale for chloroquine-resistant P. Vivaxl (Papua New Guinea, Indonesia) A drugs Medicinal Products for choice A. quinine sulfate plus one of the following options: 650 mg salt 3 times daily for 3 or 7 Tagee 10 mg salt / kg 3 times daily for 3 or 7 days e Doxycyclinf 100 mg two times daily for 7 days 2 , 2 mg / kg 2 times a day for 7 days Tetracyclinf 250 mg 4 times daily for 7 days 6.25 mg / kg 4 times daily for 7 days, or B. atovaquone / 4 Proguanilc certain adult tablets 1 times daily for 3 days <5 kg: Not Specified 5-8 kg: 2 tablets intended for children 1 times daily for 3 days 9-10 kg: 3 tablets intended for children for 3 days from 11 to 20 kg 1 times a day: one particular for adults tablet for 3 days from 21 to 30 kg 1 times a day: 2 tablets intended for adults for 3 days from 31 to 40 kg 1 times a day: three specific adult tablets 1 times daily for 3 days> 40 kg: 4 for adults certain tablets 1 time daily for 3 days or C. Mefloquinh 750 mg salt, then 500 mg 6-12 hours later, 15 mg salt / kg, then 10 mg / 6 kg 12 h later treatment plan A, B or C plus 30 mg Primaquink Base 1 times a day for 14 days 0.5 mg base / kg for 14 days seriousness 1 twice daily infection, all the plasmodium parenteral medication drugs of choice Chinidingluconatmplus one of the following options: Doxycyclinf, n Tetracyclinf Clindamycing, o 10 mg salt / kg dose in saline solution within 1 h, then a continuous infusion ion of 0.02 mg salt / kg / min within 4 h for at least 24 h or 24 mg salt / kg dose in 4 h, then infused 12 mg salt / kg every 8 hours beginning 8 hours after the initial dose Once the parasite density <1% and the patient can take oral medications, the treatment is with oral quinine doses above completes Just like for adults (except doxycycline and tetracycline, which are not used in children) or (investigational) Artesunatp a qplus the following: atovaquone / Proguanilc Doxycyclinf, n Clindamycing, o Mefloquinh After the "new drug protocol" in the test phase (contact CDC information about drugs and the dosage) Just as for adults (with the exception of doxycycline, which is not used in children) prevention of relapses: Only P. vivax and P. ovale drug of choice primaquine 30 mg p.o. Base 1-mal täglich für 14 Tage nach Verlassen der endemischen Region 0,5 mg Base/kg p.o. 1-mal täglich für 14 Tage nach Verlassen der endemischen Region a Nebenwirkungen und Kontraindikationen der Medikamente gegen Malaria für Nebenwirkungen und Kontraindikationen. Wenn sich Malaria während einer prophylaktischen medikamentösen Behandlung entwickelt, sollte das Medikament nicht als Teil des Behandlungsschemas verwendet werden. bDie pädiatrische Dosierung sollte die Dosis für Erwachsene nicht überschreiten.