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Lymphatic filariasis and onchocerciasis are parasitic helminth diseases that constitute a serious public health issue in tropical regions. The filarial nematodes that cause these diseases are transmitted by blood-feeding insects and produce chronic and long-term infection through suppression of host immunity. Disease pathogenesis is linked to host inflammation invoked by the death of the parasite, causing hydrocoele, lymphoedema, and elephantiasis in lymphatic filariasis, and skin disease and blindness in onchocerciasis. Most filarial species that infect people co-exist in mutualistic symbiosis with Wolbachia bacteria, which are essential for growth, development, and survival of their nematode hosts. These endosymbionts contribute to inflammatory disease pathogenesis and are a target for doxycycline therapy, which delivers macrofilaricidal activity, improves pathological outcomes, and is effective as monotherapy. Drugs to treat filariasis include diethylcarbamazine, ivermectin, and albendazole, which are used mostly in combination to reduce microfilariae in blood (lymphatic filariasis) and skin (onchocerciasis). Global programmes for control and elimination have been developed to provide sustained delivery of drugs to affected communities to interrupt transmission of disease and ultimately eliminate this burden on public health.

A rare variant of Leishmaniasis is Localized Leishmania Lymphadenitis which has been occasionally reported from south-eastern parts of Iran. So far, no molecular assay has been performed for diagnosing this variety of Leishmaniasis. Nineteen lymph node paraffin blocks were collected from 1994 to 2007. Parasite load count and histopathological patterns reported on Hematoxylin-Eosin and Giemsa stained slides.DNA extraction was carried out just on the remaining available 7 lymph node paraffin blocks according to QIAamp DNA FFPE kit instructions. A pair of primers and a probe were designed for rRNA ITS region with Allele ID 6.0 software, followed by real time PCR amplification. The most common histopathological pattern was necrotizing granuloma with few Leishman bodies. Parasite load was the highest in submental lymph node (3 ± 1.41 per oil field) which was significantly higher compared to cervical and inguinal nodes (P < 0.05). Absolute load of parasite DNA was detectable in all 7 cases. The positive cases revealed a 201 bpamplicon after electrophoresis of end product which was confirmative for Leishmania tropica. Real time PCR revealed Leishmania tropica as the etiologic agent of Localized Leishmania Lymphadenitis. Although this molecular method is a sensitive diagnostic tool, histopathological findings are still important.

CLINICAL PRESENTATION This 33-year-old man presented to our outpatient clinic with acute watery diarrhoea and abdominal cramps of 3 days duration suggesting an acute flare of Crohn's disease.

Aims: To formulate evidence based histopathological criteria for the diagnosis of acquired toxoplasmic lymphadenitis, in an area of high tuberculosis prevalence. Methods: Multiple histopathological parameters were assessed in a consecutive sample of biopsies from 68 patients presenting with lymphadenopathy with a duration of less than six months. Serum IgM enzyme linked immunosorbent assay was used as the standard reference test for the diagnosis of toxoplasmic lymphadenitis. The sensitivity, specificity, and likelihood ratios of various histological parameters were estimated. Results: The presence of microgranulomas (p < 0.0001), paracortical widening (p  =  0.006), paracortical hyperplasia (p  =  0.02), monocytoid B cells in sinuses (p  =  0.007), lower than grade 2 macrogranuloma (p  =  0.002), and the absence of giant cells (p  =  0.05) were found to discriminate between IgM positive cases and IgM negative controls. Using a composite criterion—(1) presence of microgranulomas, (2) lower than grade 2 macrogranuloma, (3) absence of giant cells, and (4) follicular hyperplasia—toxoplasmic lymphadenitis can be diagnosed with a high degree of sensitivity (100%), specificity (96.6%), and positive likelihood ratio (29). Conclusion: Toxoplasma lymphadenitis can be diagnosed with a high degree of confidence using the specific histopathological criteria identified here.

Congenital transmission of Toxoplasma gondii from a mother who was apparently immunologically competent and who had toxoplasmic lymphadenitis 2 months before conception is described. Since no T. gondii-specific serological data were available for this mother from the time her lymph node biopsy specimen was obtained, the specimen was studied by polymerase chain reaction (PCR) to determine whether the T. gondii B1 gene was present. The predictive diagnostic value of histologic findings previously considered to be classic signs of T. gondii lymphadenitis also was studied. This was done by correlation of serological tests diagnostic of acute acquired T. gondii infection and presence of characteristic findings in biopsy specimens from persons without known immunocompromise. Both PCR and review of the characteristic features of her lymph node biopsy specimen confirmed the diagnosis of preconceptual infection in the mother. We also discuss two other cases in which apparently immunologically competent mothers with preconceptually acquired infection transmitted this parasite to their fetuses.

The common site of infestation by this parasite in human digestive tract is the ileocaecal area. 1 Involvement of the small intestine, especially the jejunum, is rare; there are only a few case reports. 2 - 4 In most of the cases involvement of small intestine is seen with ileocaecal/colonic involvement. Perforation is rarely reported with severe amoebic colitis. 3 4 Factors leading to tissue invasion by virulent strains are poorly understood, and it is believed that a combination of genetic and environmental factors (changes in intestinal flora and diet) may play a role in killing of host cells. 1 Virulent E histolytica trophozoites are capable of penetrating intact intestinal mucosa; they are not opportunistic and do not require an already damaged mucosa. 1 Differentiation from non-pathogenic strains (E dispar) can be done by zymodenes and using monoclonal antibodies for galactose PP adhesin for pathogenic and non-pathogenic strains. 1 Spread to extraintestinal sites, such as liver, lung and brain, due to vascular invasion has been well documented in the literature, 1 5 but spread to draining lymph nodes due to lymphatic invasion has only been reported in a single case, where spread of trophozoites to mesenteric lymph nodes was noted in a patient with severe narcotising colitis. 6 The child in the present case report was malnourished, which probably lead to decreased immunity and a fulminant lesion, with spread to draining lymph nodes.

The purpose of this study was to determine the value of conventional and newer serological tests (toxoplasmic serological profile) in the diagnosis of toxoplasmic lymphadenitis (TL). We studied 40 consecutive patients with biopsy-proven TL. Cervical, axillary, or occipital adenopathy was present in 72.5%, 20%, and 7.5% of the patients, respectively. Low-grade fever, fatigue, general malaise, or sore throat were present in only 6 (15%) of the 40 patients. A positive result for all serological tests was time dependent from the clinical onset of lymphadenopathy. The initial serum samples were positive for antibody for each patient, as shown by a Sabin-Feldman dye test. Between 3 and 6 months after clinical onset of TL, all of the patients had antibody titers of ⩾1:1,024. The ELISA was positive for IgM antibodies in all of the patients in the first 3 months. Detection of IgA or IgE antibodies or an acute pattern in the differential agglutination test was helpful in diagnosing TL in those patients who had negative, low-positive, or equivocal titers of IgM antibodies (as measured by ELISA) after 3 months. A toxoplasmic serological profile on the first serum specimen drawn after clinical onset of TL had a sensitivity of 100%. It is advisable to obtain such a serological profile in cases of asymptomatic lymphadenopathy before biopsy is carried out, especially for those individuals who have negative or equivocal IgM antibody titers.

Histiocytic necrotizing lymphadenitis (Kikuchi's disease) is a cause of benign lymph node enlargement; this disease is not well recognized by clinicians in the Western Hemisphere. The origin of the disease is unknown, although infectious agents are suspected. We describe the first case of Kikuchi's disease of toxoplasmic origin, and we also report the results of polymerase chain reaction (PCR) analysis and immunofluorescence for detection of Toxoplasma species in lymph nodes.

Onchocerciasis - infection by Onchocerca volvulus - has four cardinal manifestations: dermatitis, subcutaneous nodules, sclerosing lymphadenitis, and eye disease. The first three are discussed here. The dermatitis begins when microfilariae degenerate in the dermis. This process is accompanied by inflammation, with degranulation of eosinophils and deposition of the major basic protein of the eosinophil granules on the cuticle of the microfilariae. So far as is known, the chronic effects of onchocerciasis are all a consequence of the degeneration of microfilariae. Subcutaneous nodules contain coiled adult worms and have an outer layer of fibrous scar and a central inflammatory cell exudate, which may cavitate. Perfusion of India ink reveals arborization of capillaries around adult worms, which derive nutrition from these networks. Onchocercal lymphadenitis is characterized initially by histiocytic hyperplasia and follicular atrophy and later by fibrosis and obstruction of lymph flow, a condition causing adenolymphocele (\"hanging groin\") and elephantiasis of the genitalia. Some patients appear to have immune tolerance to degenerating microfilariae, perhaps as a result of exposure in utero to microfilarial antigens in the maternal circulation. In contrast, other patients (Yemenites, for example) have a localized but intense response to a few microfilariae; these patients are hypersensitive - perhaps because they were not exposed to microfilarial antigens in utero. Autopsy data on infection of deep organs are limited.