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According to the WHO Malaria Report 2019 a total of 229 million people fall ill with malaria each year and two thirds of deaths involve children under 5 years of age.To review the fundus changes in the context of malaria and the importance of ophthalmoscopy in the diagnosis.Summary of changes in cerebral malaria visible on fundus examination, possible underlying pathomechanisms and the value of ophthalmoscopy in practice.Retinal findings in malaria include white or gray staining of the retina (retinal whitening), color change of retinal vessels (orange or white staining), hemorrhages often with a white center, such as Roth's spot and papilledema.The retinal changes in malaria are specific and may help to differentiate malaria from other causes of coma and fever. Smartphone-based fundus photography and artificial intelligence could support malaria diagnostics particularly in resource-poor regions.HINTERGRUND: Laut WHO Malaria Report 2019 erkranken jährlich 229 Mio. Menschen an Malaria. Zwei Drittel der Todesfälle betreffen Kinder unter 5 Jahren.Überblick über die Fundusveränderungen im Rahmen der okulären Veränderungen bei Malaria, den Stellenwert der ophthalmologischen Diagnostik und die Bedeutung der Fundoskopie bei der Diagnose.Zusammenfassende Darstellung der fundoskopisch sichtbaren Veränderungen bei zerebraler Malaria, möglicher zugrunde liegender Pathomechanismen sowie der Stellenwert der Fundoskopie in der Praxis.Bei Malaria im Fundusbild erkennbar sind eine Weiß- bzw. Graufärbung der Retina („retinal whitening“), Farbveränderung retinaler Gefäße (Orange- oder Weißfärbung), Hämorrhagien, oft mit weißem Zentrum ähnlich den Roth-Flecken sowie ein Papillenödem.Die retinalen Veränderungen bei Malaria sind charakteristisch und können helfen, Malaria von anderen Ursachen von Koma und Fieber abzugrenzen. Smartphone-basierte Fundusfotografie und künstliche Intelligenz könnten in ressourcenarmen Regionen zur Diagnose beitragen.

Cerebral malaria with Plasmodium vivax is uncommon. Normally Plasmodium falciparum is the cause of cerebral malaria. We report about a 18 year old patient from Pakistan with a history of intermittent fever for several months. The patient recovered within a few days; however prognosis can be severe when cerebral malaria is complicating the course of Plasmodium vivax infection.

Malaria plays an important role as a dangerous imported infection in Europe. In addition, the number of elderly travellers is increasing. We examined the hypothesis, whether age can be considered as a risk factor for the development of complications in malaria.We examined retrospectively 134 case records of patients of all age groups with a plasmodial infection. We analysed personal data, travel details and patient histories, the neurological status, respiratory function, as well as haematological, biochemical and parasitological parameters.There is significant evidence for a correlation between age and the frequency of complications in malaria like cerebral involvement, respiratory failure, renal failure, anaemia, and hyperparasitaemia. Out of 132 patients over 15 years of age, 49 (37.1 %) developed a severe course of malaria. In the age group of 60 years and above this percentage increased to 61.5 %. The age distribution in the group with severe malaria was significantly shifted towards the elderly (p = 0.016 in Mann-Whitney test). The duration of hospitalisation also increased with age from an average of five days for the group below 45 years to 21 days for the elderly of 60 years and above.Our findings suggest a higher risk for a severe course of malaria in the elderly. For this reason, extensive advice on the correct use of exposure- and chemoprophylaxis of malaria is especially important for travellers above the age of 60.

A 57-year-old white man had been travelling in Kenya for vacation until 14 days before admission. Due to apprehension about side effects, the patient had refused any malaria prophylaxis. Ten days before admission he developed low grade temperatures and suffered from pain in the limbs, from nausea and vomiting. A new episode of tachyarrhythmia was diagnosed two days before admission and was treated by his general practitioner. Finally he was admitted to our hospital because of high temperatures, chills and progressive clinical deterioration. Autopsy revealed prominent congestion of liver, spleen and cerebral vessels as well as subdural and subarachnoidal hemorrhage.In both thin and thick peripheral blood smears Plasmodium parasites were demonstrated in approximately 30% of the eryhthrocytes and the diagnosis of Plasmodium falciparum was immediately confirmed by an immunological test.Due to the fulminant clinical and neurological deterioration with progressive hypoxaemia, the patient required ventilator therapy already one hour after admission. Therapy with chinine and doxycycline was initiated and exchange transfusion was considered. However, due to hyperkalaemia and cardiac arrest, the patient died 4 hours after admission due to parasitic hemolysis.Severe Plasmodium falciparum infection in non-immunized patients is a medical emergency and requires immediate diagnosis and treatment. Malaria should always be considered in the differential diagnosis in persons who have travelled to endemic areas and presenting not only with temperatures, but also with non-specific clinical signs, like cardiac arrhythmias. Although never entirely effective, chemoprophylaxis is highly recommended.

Neuropsychiatric complications in the course of plasmodium falciparum infection are usually summarized as cerebral malaria. Heterogeneous clinical symptoms, different courses and inconstant parasitemia, however, suggest different pathogenic mechanisms. We report a case of an acute symptomatic psychosis occurring two weeks after successful therapy of a primary manifestation of plasmodium falciparum infection. The diagnosis of meningoencephalitis was based on lymphocytic pleocytosis of cerebrospinal fluid and hyperintense lesions in cranial magnetic resonance imaging. Due to the lack of plasmodium falciparum parasitemia and of serological evidence of viral infection a final diagnosis was not possible. Considering the pertinent literature, an immune-mediated complication of plasmodium falciparum infection (acute disseminated encephalomyelitis, ADEM) appears to be more probable than a direct viral or plasmodium CNS infection. We propose to reverse the term cerebral malaria for the cases with direct pathogenic influence of plasmodium falciparum, and to distinguish it from cases with possible immune-mediated pathogenesis.

In a retrospective study we analyzed the clinical and blood chemical data of 12 patients with severe tropical malaria in the intensive care units of the University Hospital Zurich and the Stadtspital Triemli, Zurich, between 1991 and 1994. None of the 12 patients had been exposed to malaria before or had taken drugs for chemoprophylaxis. 7 patients survived, 5 died from complications of malaria. According to the criteria of severe tropical malaria defined by the WHO, the following pathological clinical and blood chemical parameters were noted on admission: cerebral coma (2/12); blood hemoglobin5 g/dl (0/12),8 g/dl (2/12); serum creatinine265 mumol/l (3/12); blood glucose2.2 mmol/l (0.12); circulatory collapse/shock (0/12); bleeding/signs of disseminated intravascular coagulation in laboratory tests (4/12); acidosis with pH7.25 (1/12). Further signs of severe tropical malaria were: hyperparasitemia5% (9/12); qualitative and quantitative disturbances of consciousness (6/12); thrombocytopenia30 x 10(9)/l (9/12); hyponatremia 125-135 mmol/l (9/12),125 mmol/l (2/12); rhabdomyolysis with creatine kinase1000 U/l (4/12). The basic treatment consisted of parenteral quinine hydrochloride in all patients; doxycycline was added in 8 cases, clindamycin in 3. Adjuvant therapy with desferrioxamin was given in 3 cases. 6 patients had exchange transfusions. Parasitemia cleared in all patients within 5 to 6 days. Later in the course, 5 patients developed acute respiratory distress syndrome, 6 required hemofiltration due to oliguria, and one became comatose.(ABSTRACT TRUNCATED AT 250 WORDS)

Thirteen days after returning from a four week holiday in Kenya a 35-year-old man consulted his doctor complaining of feeling unwell. The doctor diagnosed influenza and gave him a sickness certificate for three days. Because the patient did not reappear at his workplace a search was made and he was found dead in his flat seven days after seeing his doctor. A medicolegal autopsy was performed two days after the estimated time of death. There was marked swelling of liver and spleen together with jaundice and "dirty grey" colouration of the viscera. Samples of heart blood and spleen puncture material were taken. Giemsa stained preparations (ordinary and thick blood smears) revealed numerous objects 1.2 to 1.5 microns in size with indistinct reddish blue staining, some of them arranged in rosettes reminiscent of schizonts. A few of them contained pigment. In material from the spleen there were masses of blackish-brown pigment. The malaria immunofluorescence test performed on serum gave a weakly positive titre of 1:40. The findings were considered enough to support a diagnosis of fulminant falciparum malaria, and this was confirmed by histological changes in various organs, notably the typical capillary blockages in the brain. Because of the popularity of long-haul tourism, cases of imported malaria are increasingly frequent and, in view of the insidiously progressive course of the disease, it should always be considered in the differential diagnosis. In cases of unexplained death, if there is any suspicion of malaria, blood should always be taken for appropriate investigations, in addition to blocks for histological examination.

The literature dealing with the psychiatric consequences of malaria is the result of the experience of physicians in former colonial countries and in both World Wars. The psychopathological categories employed in their descriptions, whether due to a lack of psychiatric expertise or the influence of the noncommittal Anglo-Saxon psychopathological nomenclature of that time, are of a wide and heterogeneous spectrum. A detailed critical comparison demonstrated that there are two fundamental forms of psychic disorders caused by malaria: 1) the pseudo-neurotic or pseudo-psychopathic alterations evidencing a varied phenomenological character, with no delimitation to the psychoses; on the contrary, with frequent transitions to them, and 2) the exogenous malaria-psychoses caused by the illness itself or occasionally resulting from a liver insufficiency or from one of many forms of cerebral involvement. The latter can terminate in either a lethal coma or a demential state. Furthermore, both endogenous psychoses apparently triggered by malaria and exogenous psychoses caused by anti-malaria drugs still exist.

By means of 5 case reports the successful use of an new blood schizontocide against plasmodium falciparum infections is demonstrated. The local patients with severe malaria were treated in the German UN-hospital in Cambodia. Cerebral, pulmonary and haemolytic complications dominated. Intramuscularly artemether, a synthetic Qinghaosu-derivative, was combined with already used antimalarials. All patients survived, regained consciousness and were without fever after administering artemether within 48 to 72 hours. The complications were controlled by mandatory ventilation, blood transfusions, fluid balance and blood sugar monitoring. With artemether we will get a well tolerated and quickly effective schizontocide. In order to avoid recrudenscence and fast drug resistance it should be combined with a tetracycline and in consequence supplemented through a second schizontocide.

Infections with malaria are increasing in Europe and Northern America and are also spreading in tropical endemic areas. A falciparum variety of malaria known as cerebral malaria is the most well-known neurological complication, caused by Plasmodium falciparum and characterised by a fulminant course with disturbances of consciousness and facultative seizures or focal neurological deficits. 50% of deaths caused by malaria are due to cerebral involvement. Pathologically a disseminated vasculomyelinopathic disorder is seen. Immunological changes, vascular-hypoxic disturbances and metabolic-toxic factors contribute to these pathological findings. Facts on diagnostic, differential diagnostic and therapeutic procedures are presented. Beside the severe and life-threatening cerebral malaria some unspecific cerebral symptoms are seen, such as cerebellar ataxia and chorea. Spinal disease and peripheral nerve involvement, polyradiculitis and especially psychiatric disorders have also been described. Every neurological and psychiatric disorder presented first in tropical areas or malaria-endemic regions requires malaria diagnostic tests. In our geographical region, any previous history of a journey to the tropics is an important pointer; in particular, neurological or psychiatric symptoms can be important pointers to malaria.