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 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Specific treatment of canine babesiosis consists of antibabesial drugs and, in severely anaemic animals, blood transfusion. Supportive therapy is also required, particularly in animals with complicated disease. Strategies for treatment of uncomplicated and complicated babesiosis are discussed. Definitive recommendations cannot be provided on the basis of available information, but suggestions are made, based on accepted therapeutic principles, pathophysiological mechanisms, therapy used in human malaria, and clinical experience. The problems of fluid therapy in complicated babesiosis, particularly in animals with oliguria, cerebral babesiosis and pulmonary oedema, are presented, with consideration given to the use of hypertonic fluids. The benefits of bicarbonate and alternative alkalinisers in life-threatening lactic acidaemia, a relatively common occurrence in complicated babesiosis, are debated, as are the benefits of oxygen therapy in anaemic hypoxia. Drug therapy and management of specific babesial complications are discussed. The rationale for supportive drugs commonly used in uncomplicated babesiosis, including lipotropic agents, haematinics and glucocorticoids, is examined. This review is designed to propose therapeutic guidelines and to stimulate interest in problematic aspects of supportive therapy for canine babesiosis.
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PMID:Supportive treatment of canine babesiosis. 854 69

Severe Falciparum malaria is associated with multiple organ dysfunction and a high rate of fatal outcome. Appropriate antimalarial chemotherapy and symptomatic treatment may be supplemented by early plasma exchange. Two cases are reported in which there were no chemoprophylaxis and a late diagnosis. Initial parasitaemias were 17% and 5%. The two patients had cerebral malaria with in the first case pulmonary oedema and DIC. Plasma exchange was performed and clinical biological symptoms abated quickly. The mechanisms of action and benefits of plasma exchange are discussed.
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PMID:[Plasma exchange and severe Plasmodium falciparum malaria. Apropos of 2 cases]. 856 56

Increasing drug resistance in Plasmodium falciparum and a resurgence of malaria in tropical areas have effected a change in treatment of malaria in the last two decades. Symptoms of malaria are fever, chills, headache, and malaise. The prognosis worsens as the parasite counts, counts of mature parasites, and counts of neutrophils containing pigment increase. Treatment depends on severity, age of patient, degree of background immunity, likely pattern of susceptibility to antimalarial drugs, and the cost and availability of drugs. Chloroquine should be used for P. vivax, P. malariae, and P. ovale. P. vivax has shown high resistance to chloroquine in Oceania, however. Primaquine may be needed to treat P. vivax and P. ovale to rid the body of hypnozoites that survive in the liver. Chloroquine can treat P. falciparum infections acquired in North Africa, Central America north of the Panama Canal, Haiti, or the Middle East but not in most of Africa and some parts of Asia and South America. In areas of low grade resistance to chloroquine, amodiaquine can be used to effectively treat falciparum malaria. A combination of sulfadoxine-pyrimethamine is responsive to falciparum infections with high grade resistance to chloroquine. Mefloquine, halofantrine, or quinine with tetracycline can be used to treat multidrug-resistant P. falciparum. Derivatives of artemisinin obtained from qinghao or sweet wormwood developed as pharmaceuticals in China are the most rapidly acting of all antimalarial drugs. Children tend to tolerate antimalarial drugs well. Children who weigh less than 15 kg should not be given mefloquine. Health workers should not prescribe primaquine to pregnant women or newborns due to the risk of hemolysis. Chloroquine, sulfadoxine-pyrimethamine, quinine, and quinidine can be safely given in therapeutic doses throughout pregnancy. Clinical manifestations of severe malaria are hypoglycemia, convulsions, severe anemia, acute renal failure, jaundice, pulmonary edema, cerebral malaria, shock, and acidosis. Health workers should be prepared to treat these symptoms accordingly.
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PMID:The treatment of malaria. 904 53

Rhabdomyolysis was diagnosed in two dogs with babesiosis. The first animal presented with muscle pain and caramel-coloured urine, and had markedly elevated serum myoglobin and muscle enzymes. Acute renal failure complicated the clinical picture. The second dog exhibited muscle pain and tremors, together with neurological signs and pulmonary oedema, and died soon after admission. Muscle necrosis and haemorrhage were found at necropsy. In human malaria, a disease clinically similar to canine babesiosis, rhabdomyolysis is unusual, but clinically silent muscle damage appears to be common. Likewise, biochemical evidence of muscle damage is readily found in experimental bovine babesiosis. Muscle enzymes were mildly elevated in three dogs with severe babesiosis and pigmenturia but there was no obvious muscle damage, indicating that this might also apply to canine babesiosis. The pathogenesis of infection-associated rhabdomyolysis and acute renal failure remains unclear, but inflammatory cytokines and nitric oxide could play an important role.
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PMID:Rhabdomyolysis as a complication of canine babesiosis. 896 83

32 cases (21 acute severe malaria and 11 chronic malaria syndrome), who developed unusual complications and/or manifestations are reported. The acute manifestations were unexplained tachypnoea 4, pulmonary oedema 5 and shock due to multiple organ dysfunction syndrome 3, melena 2 and E coli septicaemia in one. The other features were concomitant salmonellosis 2, meningitis 1, renal failure 3, hepatorenal syndrome 2, hepatitis like illness 7, neck stiffness with normal CSF 3, urticaria and subconiunctival haemorrhage 2 each, apyrexial spell with anaemia 4, thromocytopenia 3, and hypoglycaemia 3 (two pretreatment and one while on quinine in 5% glucose drip). The chronic syndrome noted were hyperreactive malaria syndrome (Tropical splenomegaly) 3, repeated haemolysis 2, chronic simple malaria with positive parasitaemia and normal Igm levels 4, and cerebellar ataxia with tremors 3. Bone marrow in these cases was hypercullular with increase plasma cells. Liver biopsy revealed lymphocytic infiltration. There was no case with permanent neurogical deficit. All patients with pulmonary oedema and multiple organ dysfunction died but chronic syndrome patients recovered fully. Early recoginition of atypical manifestation and prompt treatment will decrease the mortality and morbidity due to malaria.
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PMID:Unusual acute and chronic complications of malaria. 928 1

Malaria remains an overwhelming problem in tropical developing countries, with 300 to 500 million new cases and 1.5 to 3.5 million deaths per year. Malaria is a potentially life-threatening disease for travelers to the tropics. Imported malaria is an important clinical problem in nonendemic areas of the world because of increasing numbers of travelers, overseas workers, and immigrants from endemic areas. According to the World Health Organization's criteria, the recognition of one or more of the following clinical features should raise the suspicion of severe malaria: cerebral malaria (unrousable coma), severe anemia (hemoglobin <5 g/dL), renal failure (serum creatinine >3 mg/dL), pulmonary edema or adult respiratory distress syndrome, hypoglycemia (glucose <40 mg/dL), circulatory collapse or shock, disseminated intravascular coagulation, repeated generalized convulsions, acidosis (pH <7.25), macroscopic hemoglobinuria, hyperparasitemia (>5 percent of the erythrocytes infested by parasites), or jaundice (bilirubin >3 mg/dL). Although only a small proportion of patients with malaria develops severe manifestations, these patients require the most urgent and intensive care. Mortality among patients with cerebral malaria, even when treated in modern intensive care units, exceeds 30%, and when complicated by the adult respiratory distress syndrome, it may approach 80%. Among travelers, mortality remains a serious issue because of failure to obtain and use preventive measures, delay in seeking medical attention, and misdiagnosis.
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PMID:Imported severe falciparum malaria in Israel. 977 25

Six patients with severe and complicated falciparum malaria (6.7 +/- 2.7 WHO criteria) were admitted to our Intensive Care Unit. All patients acquired the disease while travelling in tropical Africa without appropriate chemoprophylaxis. The clinical manifestations included hyperpyrexia (all patients), chills (4), sweating (2), asthenia (3), anorexia (2), headache (1), arthralgias (1), vomiting (4), diarrhoea or abdominal discomfort (3), jaundice (2) and disturbances of consciousness (4). All patients had anemia, thrombocytopenia, hyponatremia, hypoproteinemia, hypoalbuminemia, hypocalcemia and acute renal failure, in one case associated with anuria. A low grade parasitemia was observed in two patients and a high grade parasitemia (20%-58% of erythrocytes) in four. Exchange transfusion was performed only in high parasitemic patients and all of them survived. All patients were treated with quinine, a sulfonamide and pyrimethamine. Additionally, five patients received oxytetracycline, doxycycline or clindamycin. Three patients required hemodyalisis. Five patients had delirium, coma or seizures. All patients had at least one sign of hepatic impairment: liver enlargement, jaundice or increased bilirubin or aminotransferase levels. Two patients had spleen enlargement. Laboratory findings suggested disseminated intravascular coagulation in four patients. Four patients developed pulmonary changes and three of them required mechanical ventilation. A Swan-Ganz catheter was placed in four patients. In three of them (two with pulmonary edema) the pulmonary capillary wedge pressure was initially increased, which suggested a cardiogenic or hypervolemia mechanism, but soon returned to normal level. One patient with low grade parasitemia died because of adult respiratory distress syndrome after 18 days. In our series, the degree of parasitemia was not related to the severity of the disease.
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PMID:[Severe and complicated malaria. Report of six cases]. 977 80

Pulmonary edema is a serious complication of falciparum malaria that usually occurs in association with cerebral malaria, acute renal failure, high parasitemias, or delayed antimalarial treatment. From 1993 to 1996, 120 adult patients admitted to the intensive care unit of the Bangkok Hospital for Tropical Diseases were enrolled in a prospective study to assess the combination of artesunate and mefloquine for the treatment of cerebral malaria. Twenty-five patients (21%) presented with pulmonary edema and a majority developed complications in other organs as well, especially acute renal failure. In most patients (19 of 25), pulmonary edema was noted on the first day of admission and was associated with higher parasitemias and levels of acidemia, than in patients without pulmonary edema. Ten of the 25 patients diagnosed with pulmonary edema developed signs consistent with adult respiratory distress syndrome (ARDS). The mean central venous pressure when pulmonary edema was diagnosed was markedly lower in ARDS than in non-ARDS patients, supporting the argument that fluid imbalance is not essential for malaria-induced lung injury. Seven of 10 patients with ARDS died, 5 within 24 hours of admission, but there were no deaths in the 15 pulmonary edema patients without ARDS. Early diagnosis and prompt treatment remain important principles to reduce the morbidity and mortality associated with complicated falciparum malaria. This report emphasizes that ARDS, when concurrently occurs, is a poor prognostic clinical indicator in cerebral malaria.
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PMID:Pulmonary edema in cerebral malaria patients in Thailand. 1043 53

Malaria remains today one of the major health problems in the tropics with increased morbidity and mortality. The most serious complications are caused by Plasmodium falciparum, which, in contrast to the benign malarias, may progress to a life-threatening multi-system disease. Our case concerns a young woman in the 14th week of pregnancy, admitted to the ICU in a coma, with pulmonary oedema, haemolytic anaemia, renal failure and thrombocytopenia as complications of P. falciparum malaria. The case is discussed and possible explanations for the clinical picture and complications of P. falciparum malaria are given in the light of experiences from the literature.
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PMID:Management of severe and complicated malaria in the intensive care unit. 1047 May 80

A 67-year-old male was admitted with consciousness disturbance (JCS, III-200) after completing a 12-day tour to east Africa without malaria chemoprophylaxis. When he visited the hospital one day prior to the admission complaining of fever and a slightly sore throat, he did not mention the travel history. Soon after his travel history was revealed, blood films were prepared which showed abundant ring forms accompanied with a small number of trophozoites and schizonts of Plasmodium falciparum, with the parasitemia of 26%. Despite intravenous quinine infusion, first that of loading dose, his consciousness state (JCS, III-300), renal and hepatic functions and anemia (Hb, 5.8 g/dL) deteriorated progressively. Moreover, metabolic acidosis worsened with pH of 6.954, HCO3- of 3.4 mEq/L, BE of--27.0 mEq/L, PCO2 15.5 mmHg by arterial blood gas analysis, although he received a large volume of sodium bicarbonate solution. The patient died on the 4th day of his illness. According to the literature, it is suggested that the treatment of metabolic acidosis in severe faciparum malaria with sodium bicarbonate is sometimes harmful, since it can result in sodium overloading, which may then precipitate pulmonary edema/ARDS. However, alternative treatment regimens have not yet been established. Future investigation on the etiology and the proper treatment of metabolic acidosis associated with severe falciparum malaria is highly needed.
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PMID:[A rapidly fatal case of severe falciparum malaria complicated with high-level metabolic acidosis]. 1086 Mar 64


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