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Biomedical subjects

M J Reardon

Publications and source records attributed to M J Reardon.

At least 73 records · Page 4Linked to original sources
PubMed1993

Vascular injury in anterior lumbar surgery.

Anterior approaches to the lumbar spine are rapidly gaining popularity for decompressive and reconstructive procedures. A recognized hazard to this approach to the spine is possible injury to the great vessels. This retrospective study is a review of 102 consecutive anterior lumbar spinal procedures. All approaches were performed by one of two fellowship-trained vascular surgeons. Both have extensive experience with this approach. All injuries to the inferior vena cava, common iliac vein, or other great vessels that required suture repair were recorded. The authors were surprised to note an overall rate for this vascular complication of 15.6%. These injuries included 11 tears of the common iliac vein, four tears of the inferior vena cava, and one avulsion of the iliolumbar vein. Two different approaches were used during this study. Twenty-six cases were performed through a flank incision, with the dissection proceeding through the external and internal oblique muscles as well as the transversus abdominis. The average number of levels exposed was 2.3. Two vascular complications resulted, for an incidence of 7.7%. Seventy-six procedures were carried out through a small (5-10 cm) incision overlying the rectus abdominis muscle. The retroperitoneal space was entered through the posterior rectus sheath without division of any muscle tissue. This resulted in 14 vascular complications, for an incidence of 18.4%. Although the authors are unaware of any major long-term morbidity from this complication in their patient group, they believe feel that the true incidence of this potentially quite serious complication may be underestimated.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Papillary fibroelastoma. A right atrial presentation.

Papillary fibroelastoma is a rare cardiac tumor arising most frequently from valvular endocardium. These tumors are clinically important because of their tendency to embolize. Emphasis is therefore placed on early detection and surgical excision. We describe a case of a papillary fibroelastoma arising from the right atrium. To our knowledge, only 2 such cases have been reported in the English literature. Our case illustrates the discovery of a rare, but potentially fatal cardiac tumor, successfully removed by surgery.

Aged↗
PubMed1989

A history of sleeping sickness in Kenya.

Gambian sleeping sickness entered what is now Kenya from Uganda in about 1901 and quickly spread along the Kenyan shores and islands of Lake Victoria, reaching Tanzania in 1902. By 1910 the disease had spread 25 miles inland along the Kuja and Migori rivers and their tributaries. Sleeping sickness waxed and waned in these areas despite attempts to control tsetse fly populations by various methods. It was not until 1950, when the use of insecticides (DDT) applied by backpack sprayer proved successful against Glossina fuscipes at Kibigori, that eradication of G. fuscipes and Gambian sleeping sickness seemed possible. Subsequently the Kuja-Migori endemic area was cleared of flies and disease, as well as the South and Central Nyanza lake shores and islands. By 1965 Gambian sleeping sickness had virtually disappeared from Kenya. A more virulent form of the disease, Rhodesian sleeping sickness, may have also spread to Kenya from Uganda, although its appearance in diverse areas of the Gambian disease suggest that local ecological factors may have played a role in enhanced virulence of trypanosomes stocks. The Rhodesian form of sleeping sickness appeared in the Lambwe Valley, South Nyanza, in about 1959, and despite attempts to eradicate this disease it still persists as the only remaining endemic area in Kenya at this time. The usual transmission of Rhodesian sleeping sickness by G. pallidipes in Kenya was altered when an outbreak occurred at Alego, in Central Nyanza, in 1964. It was discovered that G. fuscipes was the vector and that domestic cattle were an important reservoir of infection. Glossina fuscipes was also the vector of Rhodesian sleeping sickness in an outbreak in Samia in 1976 and another along the lakeshore in South Nyanza in 1981. Sleeping sickness has been restricted primarily to the Western and Nyanza Provinces of Kenya (Fig. 1).

Animals↗
PubMed1989

The Lambwe Valley and its people.

By 1936 the Lambwe Valley, which had been heavily populated in the early years of this century, was nearly devoid of people. Population since that time has increased markedly as a result of a settlement scheme and efforts made to control and eradicate Glossina pallidipes and trypanosomiasis. The formation of a game reserve (now a National Park) prevented the completion of a tsetse eradication programme and has provided an unmolested habitat for both G. pallidipes and large numbers of game animals which act as a reservoir for trypanosomiasis. Rhodesian sleeping sickness, as well as animal trypanosomiasis, have been severe problems for the local farmers who live around the boundaries of the National Park.

Animals↗
PubMed1989

Sleeping sickness in the Lambwe Valley in 1978.

Even though tsetse control measures were discontinued in the Lambwe Valley in 1974 the prevalence of Rhodesian sleeping sickness remained at low levels. A survey conducted in 1978 verified a low prevalence of disease (0.1%). Thirty-four per cent of the individuals tested were positive for malaria with the highest prevalence (44%) in children aged 0-9 years. Thirteen of 1340 individuals (0.97%) tested and found negative for sleeping sickness in 1978 developed the disease by 1985. Fourteen individuals with moderate titres (2+) in the IFAT but who showed no evidence of disease were traced and found to be alive and well seven years later. Three of these patients still had positive titres but the others had converted to negative. Sera from four patients infected and treated in 1978 were also positive, but only one of five patients treated in 1977 reacted in the test. The CFT as described did not appear useful as a diagnostic test.

Adolescent↗
PubMed1989

Demographic characteristics of the Lambwe Valley population.

Thirty-four per cent of the population (11,079) in the Lambwe Valley study site was under the age of 10, and 59% were under the age of 20. The population was equally divided among males and females (M/F 0.99). The crude birth rate averaged 45%; the death rate was 8% and the natural increase averaged 37%. Infant and child mortality was 66% and 108% respectively. The average household size was 8.4 individuals. The population migrated to the Lambwe Valley primarily from other areas in Kenya, although 13% were from Tanzania. The predominant tribal group was Luo (59%) followed by the Abasuba (38%). A few Luyha and Kisii were also encountered. Population increased by 3.5-fold in the 1960s, followed by a 2.5-fold increase in the 1970s. Due to an aerial spray tsetse control programme, sleeping sickness had a low prevalence in October 1981 (one of 5749). Of 339 individuals confirmed as sleeping sickness patients by hospital records from within the study site 320 (94.3%) were traced to their homes. Mortality in domestic cattle (40%), goats (47%), sheep (55%), and dogs (50%) had occurred over the previous two years during an outbreak of trypanosomiasis.

Age Factors↗
PubMed1989

Epidemiology of Rhodesian sleeping sickness in the Lambwe Valley, Kenya.

A total of 912 cases of sleeping sickness have been recorded from the Lambwe Valley from 1959 to 1984. After a period of decreasing prevalence in the 1970s an outbreak of disease occurred between 1980 and 1984. The incidence of disease for this five-year period was highest in areas adjoining the Ruma National Park, reaching 54% in Area I. Attack rates were highest in the 50+ age group (125) and children had significantly lower attack rates (8%) in this area of peridomestic transmission. Sex ratios of patients (M/F) were near 1.0 in areas in closest proximity to the thickets in the National Park, while in distant areas the ratios rose to 6.0. The distribution of the number of patients within different households was studied; fewer households than expected had 0 or one patient, and more than expected had three or more patients. No difference in attack rates were found between Nilotic and Bantu groups. Twelve different zymodemes were found in 136 stocks of Trypanosoma brucei rhodesiense. Four new zymodemes appeared in 1980 in the latest outbreak and accounted for 73% of the stocks isolated from man during this outbreak. Neutralization tests indicated that each trypanosome zymodeme may also represent a different serodeme.

Age Factors↗
PubMed1989

Diagnosis of Rhodesian sleeping sickness in the Lambwe Valley (1980-1984).

In primary Rhodesian sleeping sickness patients, parasitological diagnosis was best performed by rodent inoculation of blood (98.5%+) followed by Giemsa-stained thick blood smears (93.3%+). Parasitological diagnosis in relapse patients was sometimes impossible and clinical diagnosis based on CSF examination was necessary. Early during a disease outbreak in 1980, 89% of the infections were detected by mobile field teams, but once established in the endemic area a stationary diagnostic facility detected most of the cases. A total number of 23,751 examinations for Rhodesian sleeping sickness and malaria were made by mobile field teams during 1980-1984; 102 primary cases (0.43%) and 25 (0.10%) relapse cases were diagnosed. A total of 9339 individuals (39%) had patent malaria infections. The IFAT was positive in 89% of the primary sleeping sickness patients and 77% of the relapse patients. Seventy-nine per cent of the primary patients were positive in a CFT test, and 77% of the relapse patients were considered positive.

Animals↗
PubMed1989

Presenting features of Rhodesian sleeping sickness patients in the Lambwe Valley, Kenya.

During a recent outbreak of Rhodesian sleeping sickness in the Lambwe Valley no asymptomatic Rhodesian sleeping sickness patients were found although 54% of the primary patients had mild symptoms and 9% were stuporous or comatose at presentation. The duration of symptoms was three months or less in 90% of the patients. Headache, weakness, joint and back pains and weight loss were claimed by at least 75% of the patients, while 82% of the females reported amenorrhoea and 70% of the males claimed impotency. Physical examination revealed lymphadenopathy in 86% but fever in only 36% of the patients, while chancres were found in only 16%. Patients had significantly lower levels of haemoglobin and thrombocytes than controls and their erythrocyte sedimentation rates were elevated. A comparison of both blood group and haemoglobin type between patients and controls yielded no significant differences. Fifty-seven per cent of the primary patients reporting mild symptoms had abnormal levels of leucocytes in their CSF. All relapse patients had abnormal CSF parameters. Levels of serum urea nitrogen were significantly elevated in patients, but SGOT, SGPT and total bilirubin were not. Levels of albumin and beta-globulin in patients were significantly lower than controls while gamma-globulin was elevated. Mean serum IgM levels in patients were elevated to nearly three-fold those of controls, but 35% of the individual patient values fell within the 95% range of control values. Some patients had extended prothrombin and thrombin times while fibrinogen levels were significantly elevated. No patients reported haemorrhage, and none was seen.

Adolescent↗
PubMed1989

Treatment of Rhodesian sleeping sickness in Kenya.

In a study of 269 sleeping sickness patients treated with Mel-B, 14 (5.2%) died during treatment. With total dosages of at least 30 ml (1.08 g), 1.4% relapsed and another 6.4% died, mostly of unknown causes, within three years of treatment, giving a success rate of 92.1% over the three years. Mel-B was used to treat 55 relapses after suramin therapy with 1.8% deaths during treatment, 3.6% relapses, and 92.7% success over at least three years. Apparent drug resistance to Mel-B was found in three patients who continued to relapse after repeated treatments. During 1980, 51 patients were treated with suramin on the basis of clinical condition without benefit of cerebrospinal fluid (CSF) analysis. Subsequently 49% of these patients relapsed within three years of treatment. When 29 patients were treated on the basis of CSF evaluation only two (7%) relapsed.

Adolescent↗
PubMed1989

Review of tsetse control measures taken in the Lambwe Valley in 1980-1984.

During an outbreak of Rhodesian sleeping sickness in the Lambwe Valley in 1980 initial tsetse control measures consisted of applications of dieldrin to the periphery of the Ruma National Park. This activity had a marked effect on the prevalence of sleeping sickness. Concern about the use of dieldrin caused the cessation of this programme and justified an aerial spray programme using endosulfan. Although the Lambwe Valley did not appear to be a good candidate for aerial spray, the endosulfan had a marked effect on tsetse fly levels and on the prevalence of sleeping sickness. Sleeping sickness cases were detected in decreasing numbers for eight months following the endosulfan programme, but the subsequent five months yielded no cases of sleeping sickness in the area. Some flies persisted, however, and they had regained high levels in about a year. As the prevalence of sleeping sickness increased another aerial spray programme was initiated in 1983, using pyrethrum as insecticide. The pyrethrum aerial spray programme did not make significant reductions in the Glossina pallidipes population or in the prevalence of sleeping sickness. A subsequent ground control programme using insecticides (dieldrin and cypermethrin) and bush clearing, conducted primarily within the National Park, has subsequently limited the prevalence of sleeping sickness to low levels.

Aerosols↗
PubMed1989

Mechanical transmission of Trypanosoma brucei rhodesiense by Glossina morsitans morsitans (Diptera:Glossinidae).

Interrupted feedings of teneral, laboratory-reared Glossina morsitans morsitans were used to study mechanical transmission of Trypanosoma brucei rhodesiense. Intervals between exposure of individual flies on parasitaemic rats and refeeding on clean rats were varied from five minutes to 24 hours. Direct transmissions were demonstrated at each interval up to 160 minutes after exposure. Proboscis dissections showed that active trypanosomes were present up to 320 minutes after exposure. No mechanical transmissions from bovine to bovine occurred in 39 attempts, when groups of 20-120 flies exposed on parasitaemic bovines were transferred immediately to uninfected cattle, but two of 40 individual flies exposed on parasitaemic bovines mechanically transmitted trypanosomes to clean rats. Proboscis dissections made immediately after flies were exposed to a bovine with a parasitaemia of 4.8 x 10(-4) trypanosomes/microliters of blood showed that 11 of 20 (55%) had active trypanosomes in the food canal. The mean number of trypanosomes per proboscis was 29.4 (+/- 20.5). Of 20 flies exposed on a bovine with a low parasitaemia, however, only one trypanosome was seen in proboscis dissections. The parasitaemia of the infected donor was an important factor in mechanical transmission. The mechanical transmission of trypanosomes from one host to another may largely depend on the infectivity threshold of the recipient host, and individual mechanically-infected tsetse flies may not transmit an infective dose.

Animals↗
PubMed1989

Experimental infection of cattle with Trypanosoma brucei rhodesiense.

Infection of cattle with various stocks of Trypanosoma brucei rhodesiense indicated that 49% developed a fatal CNS disease comparable to that found in man. Duration of disease ranged from 85 to 1613 days post infection. All eight stocks of T. b. rhodesiense tested, including those from Ethiopia and Tanzania, induced CNS disease. Blood became positive three to five days after inoculation, and after an initial peak of parasitaemia remained positive for three to five months. Subinoculation of blood into rodents subsequently became negative, although trypanosomes persisted in the lymph nodes for at least 56 to 1613 days. Only animals with CNS disease had detectable parasites in the CSF, usually after the animals had undergone severe deterioration. At post mortem examination trypanosomes could usually be found in the lymph nodes and CSF, and occasionally in the blood. Clinical signs included fever, hyperkinesia, weight loss, cerebellar ataxia, tremor, salivation and hyperaesthesia. A mild to moderate anaemia accompanied a transient thrombocytopenia and leucopenia. Animals subsequently developed leucocytosis. A pleocytosis and elevated total protein in the CSF was found, which persisted in some animals for long periods. Histopathological examination of the brain showed prominent generalized perivascular infiltrates consisting mainly of lymphocytes and plasma cells. Mott's cells were regularly observed. Vascular changes were characterized by swollen endothelium, infiltration of the vascular wall by inflammatory cells, and in some instances perivascular oedema. In the most severe cases evidence of ischaemia consisted of large numbers of astrocytes, rarefaction of the parenchyma, and areas of necrosis with loss of normal architecture. Demyelination was limited to perivascular areas. Occasionally a moderate to severe pancarditis was found.

Animals↗
PubMed1989

Cerebral trypanosomiasis in naturally-infected cattle in the Lambwe Valley, south Nyanza, Kenya.

Surveys in Zebu cattle in the Lambwe Valley in 1980 indicated that many (up to 70%) were infected with trypanosomes. The predominant parasite was Trypanosoma brucei sspl followed by T. congolense. Cerebrospinal fluid (CSF) analysis showed a high proportion of animals with pleocytosis and elevated total CSF protein. Trypanosomes were detected in CSF and signs of a central nervous system (CNS) disease were observed. Histopathological lesions in the CNS were identical to those found in experimentally-infected cattle and consisted of perivascular infiltrations, swollen endothelium of vessels, infiltration of the vascular wall, and perivascular oedema. The severest cases showed rarefaction, astrocytosis and areas of necrosis. Infected cattle transported to the Veterinary Research Laboratory were studied for up to four years. Absence of trypanosomes from the peripheral blood was common, and even subinoculation of lymph node aspirates and CSF were usually negative. Death was preceded by a period of weight loss and the development of severe CNS signs. An attempt to cure animals with Mel-B treatment failed. Serum from naturally-infected cattle neutralized T. b. rhodesiense stocks collected in the same area.

Animals↗
PubMed1989

Experimental infection of goats with Trypanosoma brucei ssp. and effects of treatment with suramin and Mel-B.

A stock of Trypanosoma brucei ssp. isolated from a naturally-infected goat in the Lambwe Valley, Kenya, induced cerebral trypanosomiasis in experimentally-infected goats. Six of nine goats with cerebral trypanosomiasis induced by this stock were cured by a single high dose of suramin (50 mg kg-1). Two other goats appeared to be cured with this dosage of suramin but later developed abnormal central nervous system (CNS) signs and parasitaemia. Parasites first appeared in the cerebrospinal fluid (CSF) and then in the blood and lymph nodes. Mel-B was also effective against primary and relapse cerebral trypanosomiasis in goats.

Animals↗