Bacteriological studies of blood, tissue fluid, lymph and lymph nodes in patients with acute dermatolymphangioadenitis (DLA) in course of ‘filarial’ lymphedema

Abstract

Filarial lymphedema is complicated by frequent episodes of dermatolymphangioadenitis (DLA). Severe systemic symptoms during attacks of DLA resemble those of septicemia. The question we asked was whether bacterial isolates can be found in the peripheral blood of patients during the episodes of DLA. Out of 100 patients referred to us with 'filarial' lymphedema 14 displayed acute and five subacute symptoms of DLA. All were on admission blood microfilariae negative but had a positive test in the past. Blood bacterial isolates were found in nine cases, four acute (21%) and five subacute (26%). In 10 acute cases blood cultures were found negative. Six blood isolates belonged to Bacilli, four to Cocci and one was Sarcina. To identify the sites of origin of bacterial dissemination, swabs taken from the calf skin biopsy wounds and tissue fluid, lymph and lymph node specimens were cultured. Swabs from the calf skin biopsy wound contained isolates in nine (47%) cases. They were Bacilli in nine, Cocci in three, Acinetobacter and Erwinia in two cases. Tissue fluid was collected from 10 patients and contained Bacilli in four (40%) and Staphylococci in three (30%). Lymph was drained in four patients and contained isolates in all samples (100%). They were Staphylococcus epidermis, xylosus and aureus, Acinetobacter, Bacillus subtilis and Sarcina. Three lymph nodes were biopsied and contained Staphylococcus chromogenes, xylosus, Enterococcus and Bacillus cereus. In six cases the same phenotypically defined species of bacteria were found in blood and limb tissues or fluids. In the 'control' group www.elsevier.com/locate/actatropica * Corresponding author. 73 (1999) 217-224 218 of patients with lymphedema without acute or subacute changes all blood cultures were negative. Interestingly, swabs from biopsy wound of these patients contained isolates in 80%, tissue fluid in 68%, lymph in 70% and lymph nodes in 58% of cases. In healthy controls, tissue fluid did not contain bacteria, and lymph isolates were found only in 12% of cases. This study demonstrates that patients with acute episodes of DLA reveal bacteriemia in a high percentage of cases. Diversity of blood and tissue bacterial isolates in these patients points to a breakdown of the skin immune barrier in lymphedema and subsequently indiscriminate bacterial colonization of deep tissues and spread to an blood circulation. W.L. Olszewski et al. / Acta Tropica

Microbiomes of Unreactive and Pathologically Altered Ileocecal Lymph Nodes of Slaughter Pigs

“…Surprisingly, in the ICLNs, Escherichia-and Pseudomonas-associated OTUs were the most abundant OTUs, with Ͼ30% of all reads generated in this study. Escherichia and Pseudomonas are known to be pyogenic organisms, as is Acinetobacter junii, having already been isolated from purulent tissues and lymph fluid (52,53). This is the first time Escherichia, Pseudomonas, and Acinetobacter species have been associated with purulence in porcine ICLNs.…”

Reactivity to bacterial, fungal, and parasite antigens in patients with lymphedema and elephantiasis.

“…Clearly, additional efforts are needed to define the specific organisms that may be associated with recurrent infections and ADL. 16 The relationship, if any, between filarial exposure and acute attacks remains unresolved. Kar and others suggested that antifilarial antibody levels decreased following an acute attack, but we did not see a relationship between antifilarial antibody levels and either the frequency or the time interval since the last attack.…”

“…According to this model, lymphatic damage associated with the presence of adult worms leads to impaired lymph flow and establishes conditions favorable for the development of secondary bacterial infections, causing further vessel damage and worsening of lymphedema. [16][17][18] The hypothesis that bacterial infections contribute to progression of ''filarial'' disease is supported by studies that show that bacteria can be isolated from the blood and lymph of persons experiencing acute attacks and that acute ADL attacks are prevented by improving skin hygiene and by treating entry lesions with topical antibiotics and antifungal creams. 12,16,19 These observations suggest that bacterial infections are a determinant of disease progression; however, they do not rule out a potential role for immune responses to filarial, bacterial or fungal antigens in triggering the inflammation associated with ADL or in the initiation or progression of processes leading to lymphedema.…”

“…[16][17][18] The hypothesis that bacterial infections contribute to progression of ''filarial'' disease is supported by studies that show that bacteria can be isolated from the blood and lymph of persons experiencing acute attacks and that acute ADL attacks are prevented by improving skin hygiene and by treating entry lesions with topical antibiotics and antifungal creams. 12,16,19 These observations suggest that bacterial infections are a determinant of disease progression; however, they do not rule out a potential role for immune responses to filarial, bacterial or fungal antigens in triggering the inflammation associated with ADL or in the initiation or progression of processes leading to lymphedema. If responses to these antigens are related to ADL and disease progression, then higher levels of immune reactivity to filarial, bacterial or fungal antigens should be evident among persons with lymphedema than among persons without disease.…”

Limb Lymph Node Response to Bone Fracture

“…[5][6][7][8] The influence of bacterial cells, with colonization of traumatized tissues, either directly from the damaged skin or reaching the site of trauma by lymphatics from the foot, should also be considered. 9 The macrophages that scavenge cellular debris, the subcellular fragments from damaged cells, the fragments of ground matrix, and vasoregulatory factors, are transported from the site of injury to the LNs and may evoke the cellular and humoral reaction.…”