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Congenital Trypanosomiasis in a Child Born in London
Abstract
A female infant of 22 months was referred to the Hospital for Sick Children, London, because of delayed psychomotor development. Extensive investigations revealed no cause, but eventually trypanosomiasis was diagnosed. The infant had not been outside the UK, but her mother came from Zaire, where the disease is endemic, but had lived in Kinshasa, where there is no sleeping sickness. It is thought that the mother may have been asymptomatically infected by a fresh‐blood transfusion four years earlier, since no other source of infection was apparent.
RÉSUMÉ
Trypanosomiase congénitale chez un enfant néà Londres
Une fillette de 22 mois a été addressée a L'Hôpital des Enfants Malades de Londres en raison ďun retard du développement psychomoteur. Des examens multiples ne révélérent aucune cause mais une trypanosomiase fut diagnostiquée. L'enfant n'avait pas été en dehors du Royaume Uni mais sa mére venait de Zaire ou la maladie est endémique; cependant, cette mére vivait à Kinshasa, oú il n'y a pas de maladie du sommeil. Les auteurs pensent que la mére avait été infectée asymptomatiquement par une transfusion de sang frais quatre ans plus tôt car il n'y avait aucune autre source ďinfection apparente.
ZUSAMMENFASSUNG
Angeborene Trypanosomiasis bei einem in London geborenen Kind
Ein 22 Monate altes Mädchen wurde wegen einer verzögerten psychomotorischen Entwicklung in das Hospital für kranke Kinder in London eingewiesen. Trotz umfangreicher Diagnostik konnte die Ursache nicht festgestellt werden, aber schließlich wurde eine Trypanosomiasis diagnostiziert. Das Kind war nie außerhalb des UK gewesen, aber seine Mutter kam aus Zaire, wo die Erkrankung endemisch ist, hatte aber in Kinshasa gelebt, wo es keine Schlafkrankheit gibt. Man nimmt an, daß die Mutter vier Jahre zuvor durch eine Frischblutkonserve asymptomatisch infiziert wurde, da sich keine andere Infektionsquelle fand.
RESUMEN
Tripanosomiasis congenita en un niño nacido en Londres
Una niña de 22 meses de edad fue ingresada en el Hospital for Sick Children de Londres debido a un retraso en el desarrollo psicomotor. Las exploraciones extensivas no revelaron ninguna etiología pero eventualmente se diagnosticó una tripanosomiasis. La niña no habia estado fuera del Reino Unido, pero su madre venia del Zaire donde la enférmedad es endemica, pero habia vivido en Kinshasa donde no hay enfermedad del suefio. Se cree qu la madre había estado infectada asintomáticamente por una transfuseón de sangre fresca hacia cuatro años ya que no era aparente ninguna otra fuente de infección.
... 22,23 Neuroimaging data of trypanosomiasis are scarce. 11,13,18,21,24 More detailed descriptions of the clinical presentation of T b gambiense sleeping sickness including imported cases are given in reviews by Duggan and Hutchinson, 20 Dumas and Bisser, 22 Edan, 25 and Boa et al, 23 and in the individual case reports cited above. It should, however, be kept in mind that due to the polymorphism of clinical signs, sleeping sickness may simulate a great number of other diseases, 21 and that the question of differential diagnosis may vary in individual patients. ...
... 45,[47][48][49][50][51] In imported cases, the increased white cell count and protein concentration often contribute to diagnosis of a neuroinflammatory disease. 8,9,18,24,52 The calculation of intrathecal synthesis after nephelometric analysis of albumin, IgG, IgA, and IgM in paired serum and CSF may represent a tool for further differential diagnosis. 53 On the basis of disease-related CSF immunoglobulin patterns, a suggested diagnosis can be ruled out, or more specific analysis can be suggested. ...
Sleeping sickness is a lethal African disease caused by parasites of the Trypanosoma brucei subspecies, which is transmitted by tsetse flies. Occasionally, patients are reported outside Africa. Diagnosis of such imported cases can be problematic when the infection is due to Trypanosoma brucei gambiense, the chronic form of sleeping sickness found in west and central Africa. The low number of trypanosomes in the blood and the non-specific, variable symptoms make the diagnosis difficult, particularly when the index of suspicion is low. When the trypanosomes have penetrated into the central nervous system, neuropathological signs become apparent but even at this stage, misdiagnosis is frequent. Rapid and correct diagnosis of sleeping sickness can avoid inappropriate or delayed treatment and even death of the patient. In this article, an overview on diagnosis of imported cases of T b gambiense sleeping sickness is given, and possible pitfalls in the diagnostic process are highlighted. Bioclinical parameters that should raise the suspicion of sleeping sickness in a patient who has been in west or central Africa are discussed. Techniques for diagnosis are reviewed. A clinician suspecting sleeping sickness should contact a national reference centre for tropical medicine in his or her country, or the WHO, Geneva, Switzerland, or the Centers for Disease Control and Prevention (CDC), Atlanta, GA, USA, for clinical consultation and provision of specific diagnostic tests. Appropriate drugs for sleeping sickness treatment are also provided by WHO and the CDC.
... 22 Congenital infection has been described in the literature. 75,76 In the majority of reported cases, maternal infection was not identifi ed, and the infant presented with a sepsis-like illness in the perina tal period. The exact route of transmission is unclear. ...
... The exact route of transmission is unclear. 75,76 Prevention includes avoiding contact with tsetse fl ies, which can bite through clothing. Typically, they infect during the daytime and are sometimes not repelled by common insect repellants. ...
With the overall increase in international travel, there is likely to be an increase in travel during pregnancy as well. In developing countries, pregnant women face exposures that can add significant risk for neonatal morbidity and mortality. Infections that can occur in utero or in the early neonatal period include malaria, yellow fever, tuberculosis, hepatitis, human immunodeficiency virus, leishmaniasis, toxoplasmosis, filariasis, Japanese encephalitis, rubella, typhoid fever, leptospirosis, dengue fever, Helicobacter pylori, and trypanosomiasis. When travel and potential exposure cannot be avoided, preventive measures are usually effective. Pretravel consultation should include careful discussion of length of travel, antimalarial prophylaxis, insect avoidance, food and water hygiene, vaccination, and body fluid precautions.
... Congenital transmission of HAT is assumed in newborns of a HAT-infected mother where the diagnosis can be confirmed within the first 5 days of life and in older children born outside an endemic country from a mother who had acquired the infection in an endemic region [1]. Eighteen cases of certain vertical transmission of HAT have been published [1,2]; only 3 were children who never entered an endemic country themselves, born to an infected mother [3][4][5]. The diagnosis of these 3 cases was delayed for months (19-24 months), as in our case, probably because the symptoms were nonspecific [6] and difficult to distinguish from other causes of psychomotor retardation. ...
... 1985 wurde in London ein Fall einer pränatalen Trypanosomose bei einem Kind, welches niemals außerhalb von England gewesen war, beobachtet. Die einzig mögliche Infektionsquelle war eine Bluttransfusion, welche die Mutter 4 Jahre zuvor erhalten hatte (LINGAM et al. 1985). Das klinische Bild bei einem infizierten Neugeborenen reicht vom Fehlen von Symptomen bis zu Bewusstseinstörungen und Krampfanfällen. ...
Tsetse flies, trypanosomes and sleeping sickness – the most fatal parasitic infection. Sleeping sickness is caused by two subspecies of Trypanosoma brucei (Euglenozoa: Kinetoplastida) and occurs solely in Africa. It is transmitted by tsetse flies (Diptera: Glossinidae), which are diurnal insects restricted to sub-Saharan Africa and small parts of the Arabian peninsula. Approximately 60 million people in 37 African countries are at risk of being infected. The highest infection rates are found in southern Sudan. Sleeping sickness, in the first stage of the disease, is a febrile illness with lymphadenopathy that progresses with the
typical symptoms of meningoencephalitis. The second stage begins when the trypanosomes break through the blood-brain barrier and invade the CNS (central nervous system). Sleeping sickness is a fatal disease – in the Eastern African form (T. b. rhodesiense) death usually occurs within several months, in the Western African form (T. b. gambiense) 1-2 years after initial symptoms. It is thus one of the very few infectious diseases with a mortality rate of 100 %. Since, even in endemic areas, only a small proportion of the tsetse population carries trypanosomes, one must remain in a risk area for a considerably long period of time to become infected. The fight against sleeping sickness still largely relies on vector control. A WHO program to guarantee the supply with therapeuticals in endemic areas gives new hope.
... 1985 wurde in London ein Fall einer pränatalen Trypanosomose bei einem Kind, welches niemals außerhalb von England gewesen war, beobachtet. Die einzig mögliche Infektionsquelle war eine Bluttransfusion, welche die Mutter 4 Jahre zuvor erhalten hatte (LINGAM et al. 1985). Das klinische Bild bei einem infizierten Neugeborenen reicht vom Fehlen von Symptomen bis zu Bewusstseinstörungen und Krampfanfällen. ...
... Three infected cases of children of 19, 22, and 24 months old with second stage HAT and born in France and England of infected mothers are also been described. The three children have never been in a HAT endemic country and vertical transmission was assumed (Lingam et al., 1985;Rocha et al., 2004). Vertical transmission of HAT is not mentioned in several examples of HAT literature. ...
FOREWORD
It is now almost fithteen years since the Pan African Tsetse and Trypanosomiasis Campaign (PATTEC) Initiative has been decided by the Head of States of Africa. Most countries have developed plans and strategies for the implementation of a national PATTEC programme; several countries have initiated action on the ground aimed at eradicating tsetse and trypanosomiasis; and two countries, Botswana and Namibia, have been successfully rendered tsetse and trypanosomiasis-free. In others countries (e.g. Guinea), some well-delimited and isolated areas are in the way of totally being tsetse and trypanosomiasis freed. In spite of these encouraging results, the Campaign is longing to be effective in many countries because of various reasons among which, the lack or insuficiency of technical capacities.
In accordance with its core functions of capacities building and training, the PATTEC coordination office has initiated a number of activities, including training to build the necessary technical capacity and competence required to carry out activities in the implementation of PATTEC projects. To support this undertaking, a Training Manual for Tsetse and trypanosomiasis eradication has been written and edited with the help of differents experts.
This Training Manual is an overview of main principles leading to the successful of a PATTEC project: from the conception, planning, and executing a project, to the strengthening of acquired results with a highlight on tsetse and trypanosomiasis control strategies.
The manual is expected to provide useful knowledge for a PATTEC project execution, to guide and support the process of capacities building in tsetse and trypanosomosis programmes.
By Hassane MAHAMAT HASSANE, PATTEC Coordinator
... Three cases of children (19, 22, and 24 months old) with secondstage HAT—born in France and England of infected mothers— are described. The three children themselves are reported not to have been in an endemic country, and vertical transmission can be assumed262728. For example, one of these children was born with hydrocephalus and second-stage HAT in Marseille, France (the mother left Chad in the fifth month of her pregnancy [26]). ...
Children with human African trypanosomiasis (HAT) present with a range of generally non-specific symptoms. Late diagnosis is frequent with often tragic outcomes. Trypanosomes can infect the foetus by crossing the placenta. Unequivocal cases of congenital infection that have been reported include newborn babies of infected mothers who were diagnosed with HAT in the first 5 days of life and children of infected mothers who had never entered an endemic country themselves.
This review systematically summarizes the literature on the vertical transmission of HAT, to our knowledge for the first time. To approach the broader aspects of the subject, articles considering the epidemiology of childhood HAT and HAT in pregnancy were also included. The HAT guidelines and technical reports of the World Health Organisation, Médecins Sans Frontières, Institut de Recherche pour le Développement, and of one endemic country were reviewed.
Publications describing congenital HAT are very limited and consist only of single case reports and small case series. Generally it is assumed to be a rare event, but it has never been systematically investigated. In two publications, it is hypothesized that congenital HAT occurs more often than suspected. Not all guidelines and not all HAT literature mention this transmission route.
The risk of vertical transmission is unknown. Awareness of congenital HAT is insufficient, and as a result opportunities for an early diagnosis in newborns may be missed. All HAT guidelines and local HAT protocols should stress that in endemic areas pregnant women should be systematically checked for HAT and that newborns of HAT infected mothers should be assessed for the disease as soon as possible. Studies on the impact of HAT on fertility and pregnancy and studies on congenital HAT are long overdue.
... The best approach to concomitant treatment should be the issue of a specifically designed study.Triolo et al., 1985; Pepin et al., 2002]; second, quite often children of sleeping sickness patients may be at higher risk of infection [Khonde et al., 1997]; and third, an infection in a family reduces the workforce and may impair the nutritional status and health of the children. The few published reports on children are mainly small-scale studies, retrospective case descriptions focussing on clinical symptoms [Debroise et al., 1968; Balint and Wenninger 1975; Le Bras et al., 1977; Buyst 1977; Cramet 1982; Triolo et al., 1985; Lingam et al., 1985; Adams et al., 1986; Buissonniere et al., 1989; Benhamou et al., 1989; Blanchot et al., 1992; Jannin et al., 1993; Kazumba et al., 1993; Koko et al., 1997; Pepin et al., 2002], describing sleeping sickness in children as a fulminant disease, particularly in young children of less than 5 years of age [Aroke et al., 1998], but very rarely dealing with the treatment outcome. Children are also said to suffer more from sequelae than adults [Cramet 1982; Triolo et al., 1985; Kazumba et al., 1993; Koko et al., 1997; Aroke et al., 1998] that may provoke growth retardation, delayed sexual maturity and poorer academic performance [Aroke et al., 1998]. ...
Diss. Naturwiss. Basel (kein Austausch). Literaturverz.
... Active case detection continues, therefore, to be key in controlling T. b. gambiense. There is evidence of transplacental transmission of T. b. gambiense (Lingam et al., 1985;Triolo et al., 1985;Rocha et al., 2004) and some evidence that this may also occur in T. b. rhodesiense (Traub et al., 1978), and isolated reports of possible sexual transmission of T. b. gambiense (Rocha et al., 2004). This passing of parasites from mother to foetus or through sexual transmission is mainly of clinical interest, however, and is unlikely to drive the epidemiology of these diseases. ...
Human African trypanosomiasis (HAT), or sleeping sickness, describes not one but two discrete diseases: that caused by Trypanosoma brucei rhodesiense and that caused by T. b. gambiense. The Gambian form is currently a major public health problem over vast areas of central and western Africa, while the zoonotic, Rhodesian form continues to present a serious health risk in eastern and southern Africa. The two parasites cause distinct clinical manifestations, and there are significant differences in the epidemiology of the diseases caused. We discuss the differences between the diseases caused by the two parasites, with an emphasis on disease burden, reservoir hosts, transmission, diagnosis, treatment and control. We analyse how these differences impacted on historical disease control trends and how they can inform contemporary treatment and control options. We consider the optimal ways in which to devise HAT control policies in light of the differing biology and epidemiology of the parasites, and emphasise, in particular, the wider aspects of control policy, outlining the responsibilities of individuals, governments and international organisations in control programmes.
Trypanosomiasis is caused by haemoflagellates of the family Trypanosomatidae, genus Trypanosoma, which parasitize blood and tissues of man and animals. Human infection is caused by two different groups of Trypanosoma. The agent of Chagas’ disease (South American trypanosomiasis) is Trypanosoma cruzi, which belongs to the group stercoraria, in which development of the organism occurs in the posterior station of the vector and transmission is by contamination with its faeces. Human African trypanosomiasis is caused by organisms of the Trypanosoma brucei group. Belonging to the salivaria, development is completed in the anterior station of the vector and transmitted by inoculation. The life cycle of these organisms involves two hosts: the definitive mammalian host and an intermediate host, an arthropod vector which constitutes the main source of infection. In African trypanosomiasis agents multiply extracellularly in the blood and interstitial tissues of the definitive host, whereas in Chagas’ disease T. cruzi only multiplies intracellularly in tissues.
Mechanisms of infection leading to fetal deathReasons for the apparent lack of association between infection and stillbirthBacterial infectionsViral diseasesProtozoal infectionsFungiEvaluationReducing infection-related stillbirthReferences
Our objective was to determine the relationship between various types of perinatal infections and stillbirths.
By use of various textbooks on perinatal infections, multiple MEDLINE searches, and the reference list of all appropriate manuscripts, the appropriate English language literature was reviewed to define the relationship between various perinatal infections and stillbirths.
Infection may cause stillbirth by a number of mechanisms, including direct infection, placental damage, and severe maternal illness. A large variety of organisms have been associated with stillbirth, including many bacteria, viruses, and protozoa. In developed countries, between 10% and 25% of stillbirths may be caused by an infection, whereas in developing countries, which often have much higher stillbirth rates, the contribution of infection is much greater. Ascending bacterial infection, both before and after membrane rupture, with organisms such as Escherichia coli, group B streptococci, and Ureaplasma urealyticum is usually the most common infectious cause of stillbirth. However, in areas where syphilis is very prevalent, up to half of all stillbirths may be caused by this infection alone. Malaria may be an important cause of stillbirth in women infected for the first time in pregnancy. The two most important viral causes of stillbirth are parvovirus and Coxsackie virus, although a number of other viral infections appear to be causal. Toxoplasma gondii, leptospirosis, Listeria monocytogenes, and the organisms that cause leptospirosis, Q fever, and Lyme disease have all been implicated as etiologic for stillbirth.
Because infection-related stillbirth is relatively rare in developed countries, and those that do occur are caused by a wide variety of organisms, reducing this etiologic component of stillbirth much further will be difficult. However, in certain developing countries, the stillbirth rate is so high and the infection-related component so great that achieving a substantial reduction in stillbirth should be possible simply by reducing maternal infections.
Infection is an important cause of stillbirths worldwide: in low-income and middle-income countries, 50% of stillbirths or more are probably caused by infection. By contrast, in high-income countries only 10-25% of stillbirths are caused by infection. Syphilis, where prevalent, causes most infectious stillbirths, and is the infection most amenable to screening and treatment. Ascending bacterial infection is a common cause of stillbirths, but prevention has proven elusive. Many viral infections cause stillbirths but aside from vaccination for common childhood diseases, we do not have a clear prevention strategy. Malaria, because of its high prevalence and extensive placental damage, accounts for large numbers of stillbirths. Intermittent malarial prophylaxis and insecticide-treated bednets should decrease stillbirths. Many infections borne by animals and vectors cause stillbirths, and these types of infections occur frequently in low-income countries. Research that better defines the relation between these infections and stillbirths, and develops strategies to reduce associated adverse outcomes, should play an important part in reduction of stillbirths in low-income countries.
Asymptomatic carriers of African trypanosomiasis are very rare but one is here reported. Although she has had no trypanosomal treatment she remains well 3½ years after leaving an endemic area and 39 months after giving birth to a child demonstrated on several occasions to be infected with trypanosomiasis. Details of the asymptomatic carrier and of other members of her family are given.
This review focuses on the parasitic diseases which occur frequently in the tropics and which affect pregnant women. Clinical disease of the mother during pregnancy, vertical transmission of parasites and transplacental passage of soluble parasitic antigens are discussed in relation to their immunopathological significance for the fetus. The incidences of congenital malaria, African trypanosomiasis and Chagas' disease are reviewed, together with vertical transmission of filarial infection, involvement of the female genital tract in schistosomiasis, and fulminant colitis due to Entamoeba histolytica infection during pregnancy.
A case of congenital trypanosomiasis due to Trypanosoma brucei rhodesiense is reported. The baby was delivered by caesarean section but the mother died three days after delivery with extensive encephalitis and renal tubular necrosis. The infant was successfully treated with Suramin and Mel-B. The IgM levels in the blood were raised during the infection but returned to normal after treatment. The macroglobulin was not detected in the CSF inspite of the presence of trypanosomes. The reasons for this are discussed.
A 17-day old baby girl presented with signs and symptoms of neonatal meningitis, except that she did not respond to the usual
drugs. Intensive investigations showed that she had trypanosomal meningo-encephalitis or sleeping sickness. Her CSF was full
of T. gambiense. Her mother's blood, but not her CSF, also contained the parasites. The clinical features and laboratory findings of the
disease in this neonate were very different from those usually found in adults.
Furthermore, her infection was complicated by the syndrome of inappropriate anti-diuretic hormone secretion. She died of the
disease and its complications probably aggravated by the drug (suramin) with which she was treated. This is believed to be
the first case of congenital trypanosomiasis described in Nigeria, and it occurred in Lagos where it was least expected.
Urn caso de doenca de sono congénita
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Trypanosomiase humaine observée chez un enfant âgé de cinq jours
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Hydrocéphalic congénitale par trypanosomiase hereditaire. Demonstration de la possibilityé du passage transplacental dans l'espéce humaine
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La trypanosomiase africaine du jeune enfant
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Sur un cas de trypanosomiase congénitale à Douala
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Un cas de trypanosomiase africaine congenitale
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Trypanosomiasis successfully treated in a pregnant woman
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Rhodesian sleeping sickness and pregnancy
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Deux cas d'héredo‐trypanosomiase
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Etude de la sympto-matologie de la trypanosomiase africaine chez l'enfant (à propose de 24 observations)
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