RESUMEN
Sustainable control of human filariasis would benefit enormously from the development of an effective vaccine. The ability to vaccinate experimental animals, with reductions in worm burden of over 70%, suggests this aim is possible. However, in experimental vaccinations the challenge is usually administered 2 weeks after the immunisation phase and thus the protection obtained is likely to be biased by persisting inflammation. Using the murine model Litomosoides sigmodontis, we increased the time between immunisation with irradiated larvae and challenge with fully infective L3 to 5 months. Significant protection was achieved (54-58%) and the reduced worm burden was observed by 10 days p.i. The developmental stage targeted was the L3, since no nematodes died once they reached the pleural cavity of vaccinated mice, as has been previously shown in short-term protocols. However, larval developmental rate was faster in vaccinated than in primary-infected mice. Immunological assessments were made prior to challenge and then from 6 h to 34 days post-challenge. Samples were taken from the subcutaneous tissue where the larvae were inoculated, the lymph nodes through which they migrate and the pleural cavity in which they establish. Eosinophils were still present although scarce in the subcutaneous tissue of vaccinated mice before challenge. Cytokine and specific antibody production of vaccinated and challenged mice were L3-specific and Th2-biased and greatly exceeded the response of primary-infected mice. The heightened Th2 response may explain the faster development of the filarial worms in vaccinated mice. Thus, long-term vaccination protocols generated a strong memory response that led to significant but incomplete protection that was limited to the infective larval stage suggesting alternative vaccination strategies are needed.
Asunto(s)
Filariasis/prevención & control , Filarioidea/inmunología , Vacunación/métodos , Vacunas/farmacología , Animales , Anticuerpos Antihelmínticos/sangre , Citocinas/genética , Citocinas/inmunología , Ensayo de Inmunoadsorción Enzimática , Eosinófilos/inmunología , Eosinófilos/parasitología , Femenino , Filariasis/inmunología , Filarioidea/efectos de la radiación , Citometría de Flujo , Humanos , Larva/inmunología , Larva/efectos de la radiación , Ganglios Linfáticos/inmunología , Ganglios Linfáticos/parasitología , Ratones , Ratones Endogámicos BALB C , Cavidad Pleural/inmunología , Cavidad Pleural/parasitología , ARN de Helminto/química , ARN de Helminto/genética , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Estadísticas no Paramétricas , Vacunas/inmunologíaRESUMEN
We report an anal metastasis from a lung cancer which was diagnosed on symptoms mimicking an acute anal abcess. The diagnosis was based on specific immunohistochemistry.
Asunto(s)
Adenocarcinoma/secundario , Neoplasias del Ano/secundario , Neoplasias Pulmonares/patología , Humanos , Masculino , Persona de Mediana EdadRESUMEN
Our aim in this study was to observe the movements of filarial infective larvae following inoculation into the mammalian host and to assess the effect of vaccination on larval migration, in situ. Here we present recordings of larvae progressing through the subcutaneous tissues and inguinal lymph node of primary infected or vaccinated mice. We used the filaria Litomosoides sigmodontis in BALB/c mice that were necropsied 6 hours after the challenge inoculation of 200 larvae. Subcutaneous tissue sections were taken from the inoculation site and larvae were filmed in order to quantify their movements. Our analyses showed that the subcutaneous larvae were less motile in the vaccinated mice than in primary-infected mice and had more leucocytes attached to the cuticle. We propose that this reduced motility may result in the failure of a majority of larvae to evade the inflammatory reaction, thereby being a possible mechanism involved in the early vaccine-induced protection.
Asunto(s)
Fístula Rectal/diagnóstico , Sarcoidosis/complicaciones , Adulto , Humanos , Masculino , Fístula Rectal/etiologíaRESUMEN
An experimental host-parasite association involving BALB/c female mice infected with Plasmodium vinckei petteri was used with the aim of investigating the morphological and physiological alterations induced by the parasite in the genital tract of the host. The vaginal oestrous cycle was monitored as a daily clue to the sexual physiology of the female mice, and a complete histological analysis of the genital tract was performed 36 days following parasite inoculation. The oestrous cycle showed strong transitory alterations during the first 30 days following infection. The occurrence of oestrus days increased during the first 10 days post-infection and then decreased to a subnormal value during the following 20 days. Infected mice also showed a remarkable hypotrophy of their clitoral glands 30 days after the beginning of the malarial infection. A probable cause of such perturbations is a significant hormonal imbalance triggered by the erythrocytic proliferation of the Plasmodium. The relationship between the immune response of the host and these physiological and morphological alterations, as well as the outcomes of these alterations on the sexuality of the rodent host are discussed.
Asunto(s)
Clítoris/patología , Ciclo Estral , Malaria/patología , Malaria/fisiopatología , Animales , Clítoris/anatomía & histología , Clítoris/citología , Femenino , Malaria/parasitología , Ratones , Ratones Endogámicos BALB C , Parasitemia/diagnóstico , Plasmodium/aislamiento & purificaciónRESUMEN
Multifocal nodular oncocytic hyperplasia of salivary glands is a tumor-like lesion that occurs predominantly in the parotid gland. The differential diagnosis of the clear cell variant includes many malignant salivary gland tumors. We report the case of a 66-year-old woman who was referred for a left total parotidectomy allowing the final diagnosis of clear cell multifocal nodular oncocytic hyperplasia. The differential diagnoses and histopathogenesis of this rare entity are discussed.
Asunto(s)
Adenoma Oxifílico/patología , Glándula Parótida/patología , Neoplasias de la Parótida/patología , Adenoma Oxifílico/cirugía , Anciano , Diagnóstico Diferencial , Femenino , Humanos , Hiperplasia , Glándula Parótida/cirugía , Neoplasias de la Parótida/cirugíaRESUMEN
Although the aetiology of Williams syndrome (WS) is related to elastin gene disruption, its pathogenesis remains unknown, particularly that of vascular lesions. The aim of the present study was to compare the elastic properties of three WS patients with age- and gender-matched normotensive and hypertensive controls. Common carotid arteries of WS patients had a higher distensibility, a thicker intima-media and a lower elastic modulus. Electron microscopy studies of one WS renal artery showed major abnormalities of the elastic fibres, which displayed a reticular structure and a thickening of the internal elastic lamina, whereas the ultrastructure of elastic fibres was normal in a control subadventitial muscular fibrodysplasia. In this WS arterial stenosis, we studied the expression patterns of several major smooth muscle (SM) phenotypic markers using immunofluorescence and used a normal renal artery as a control. In WS, SM-alpha-actin- and myosin-heavy-chain-positive cells contained low amounts of heavy caldesmon, and laminin-beta1 chain was expressed into the basement membranes, indicating a less differentiated phenotype. In conclusion, in WS patients, the carotid artery wall was abnormally distensible and thick, and major ultrastructural abnormalities of elastic fibres were observed in association with smooth muscle cell de-differentiation. These results indicate that the haplo-insufficiency of the elastin gene in WS patients leads to abnormal elastic fibre assembly within the media. Arterial wall hypertrophy found with a primary defect in elastin may represent a major factor responsible for increased distensibility. We suggest that, in WS, the increased proliferative response and the associated de-differentiation process represent two important mechanisms underlying the matrix accumulation and the development of arterial stenosis.
Asunto(s)
Arteria Carótida Común/fisiopatología , Elastina/genética , Síndrome de Williams/genética , Adulto , Presión Sanguínea , Diferenciación Celular , Tejido Elástico/ultraestructura , Elasticidad , Femenino , Humanos , Masculino , Persona de Mediana Edad , Músculo Liso Vascular/patología , Arteria Renal/ultraestructura , Obstrucción de la Arteria Renal/patología , Túnica Íntima/patología , Túnica Media/patología , Síndrome de Williams/patología , Síndrome de Williams/fisiopatologíaRESUMEN
Este estudio investiga el comportamiento de diferentes grados de neoplasia intraepitelial cervical (cervical intraepithelial neoplasia, CIN) incluyendo la relación estadística entre progresión persistencia y regresión en un gran número de pacientes. El estudio se realizó a partir de 5.782 resultados citológicos e histopatológicos de la investigación del cáncer cervical de 2.058 pacientes con CIN. Se comparó el comportamiento de diferentes lesiones de CIN y se analizaron estadísticamente las tasas de progresión, regresión y persistencia. Se detectó CIN en 5.778 muestras; 4 casos demostraron un carcinoma microinvasor del cérvix uterino. El 23 por ciento de CIN se asoció al papilomavirus humano (human papillomavirus HPV). Para todas las lesiones CIN, se observó una tasa de progresión del 12,9 por ciento. La tasa de progresión hacia la malignidad fue de 0,07 por ciento. La tasa de progresión más elevada fue para CIN I (41,9 por ciento). La progresión a CIN III/CIS fue significativamente superior para CIN II (14,5 por ciento) que para CIN I (7,5 por ciento) (test chi-cuadrado: p < 0,001). Según el estado de HPV, detectamos una progresión significativamente menor de CIN II HPV positivo (5,7 por ciento) que CIN II HPV negativo (11,6 por ciento) (test chi-cuadrado: p<0,0001). La neoplasia intraepitelial cervical en progresión es un proceso continuo. La progresión del CIN I se produce con mayor frecuencia a través de CIN II; asimismo CIN III/CIS se desarrolla más a menudo a partir del CIN II. Sin embargo, el 7,5 por ciento del CIN I mostró una progresión muy rápida hacia CIN III/CIS. Para estudiar este fenómeno se requiere investigaciones adicionales. Así mismo, se detectó una tasa notablemente baja de regresión para el CIN I y una tasa de progresión baja inesperada de CIN II HPV positivo