Disease relevance of Dysentery, Bacillary

• Here we show that casp-1(-/-) mice infected with S. flexneri do not develop the acute inflammation characteristic of shigellosis and are unable to resolve the bacterial infection [1].
• To determine the role of humoral mucosal immune response in protection against shigellosis, we have obtained a monoclonal dimeric immunoglobulin A (IgA) antibody specific for Shigella flexneri serotype 5a lipopolysaccharide (mIgA) and used a murine pulmonary infection model that mimics the lesions occurring in natural intestinal infection [2].
• Protection against reinfection with noncapsulated Gram-negative bacteria, such as Shigella, an enteroinvasive bacterium responsible for bacillary dysentery, is mainly achieved by Abs specific for the O-Ag, the polysaccharide part of the LPS, the major bacterial surface Ag [3].
• When furazolidone was compared with ampicillin, clinical illness was shortened on the average from 65 to 61 h for enterotoxigenic Escherichia coli diarrhea, from 83 to 58 h for shigellosis, from 82 to 51 h for diarrhea unassociated with a detectable agent, and from 72 to 57 h for all cases irrespective of etiology [4].
• Nitrite concentrations correlated with stool volume (r2 = 0.851) in cholera and with leukocytosis (r2 = 0.923) in shigellosis [5].

High impact information on Dysentery, Bacillary

• No significant prolongation of disease was seen in subjects with shigellosis treated with loperamide [6].
• Single-dose tetracycline therapy for shigellosis in adults [7].
• Twenty-eight infants and children hospitalized for severe shigellosis were treated orally either with ampicillin trihydrate (100 mg/kg/day administered in divided doses every six hours) or with trimethoprim-sulfamethoxazole (trimethoprim, 10 mg; sulfamethoxazole, 50 mg/kg/day in divided doses every 12 hours) for five days [8].
• Trimethoprim-sulfamethoxazole therapy for shigellosis [8].
• Nalidixic acid and oxolinic acid were noted to be quite effective in vitro against shigellae and perhaps warrant further clinical study as potential agents for therapy of shigellosis, especially in view of the appearance of isolates with multiple resistance [9].

Chemical compound and disease context of Dysentery, Bacillary

• Single-dose ciprofloxacin for shigellosis [10].
• OBJECTIVE: To determine the efficacy of azithromycin in the treatment of shigellosis [11].
• Doxycycline prophylaxis for shigellosis [12].
• Predictors of serum retinol in children with shigellosis [13].
• Coprostanol was decreased in shigellosis (12.2 +/- 8.2 versus 65.8 +/- 4.7% in controls, P less than 0.001) [14].

Biological context of Dysentery, Bacillary

• It is concluded that trimethoprim-sulfamethoxazole is the best currently available drug for treatment of shigellosis in areas where multiple antibiotic resistance of shigellae is common [8].
• The ability of Shigella to spread within and between epithelial cells is a prerequisite for causing bacillary dysentery and requires the function encoded by the virG gene on the large plasmid [15].
• Thus, immunity to shigellosis correlated to up-regulation of IFN gamma production and expression of IFN gamma receptor [16].
• Together, these results imply that monocytes migrating into the inflammatory site during the early stages of shigellosis kill S. flexneri but that during bacterial uptake, they receive virulence signals from S. flexneri which induce delayed apoptosis associated with suppression of the proinflammatory cytokine response to bacterial phagocytosis [17].
• Natural immunity to shigellosis in two groups with different previous risks of exposure to Shigella is only partly expressed by serum antibodies to lipopolysaccharide [18].

Anatomical context of Dysentery, Bacillary

• Here, we determine that the PhoP/PhoQ system also regulates virulence in the aetiological agent of bacillary dysentery, Shigella flexneri, even though this pathogen escapes from the phagosome into the cytoplasm of the host cell [19].
• Furthermore, the mean number of activated B cells that secreted anti-S. sonnei LPS antibodies was significantly higher among patients with S. sonnei shigellosis than it was among patients with non-Shigella diarrhea (2.5/10(6) cells; standard error, 1.0) and healthy subjects (5.1/10(6) cells; standard error, 2.3) (P less than 0.05) [20].
• Shigella flexneri, the aetiological agent of bacillary dysentery, induces apoptosis in macrophages which, in agony, specifically release mature interleukin-1 beta (IL-1 beta) [21].
• Children with complicated shigellosis had more polarized neutrophils with FMLP at 10(-7) and 10(-6) M (P < 0.05) and with LPS than children with uncomplicated shigellosis (P < 0.05) [22].

Gene context of Dysentery, Bacillary

• Because IGFBPs modulate the concentrations and availability of IGFs in serum, IGF-binding proteins (IGFBPs) were measured along with IGF-I and IGF-II before and after 21 days of refeeding in 22 undernourished Bangladeshi children (2-4 yr of age) with shigellosis [23].
• Apoptosis in acute shigellosis is associated with increased production of Fas/Fas ligand, perforin, caspase-1, and caspase-3 but reduced production of Bcl-2 and interleukin-2 [24].
• Shigellosis was not associated with increased humoral IL-1 beta, endotoxin, or antigen-antibody complexes [25].
• Blockade of CD14 aggravates experimental shigellosis [26].
• It is possible that intracerebral production of TNF alpha and IL-1 beta plays a role in neurological disturbances of human shigellosis [27].

Analytical, diagnostic and therapeutic context of Dysentery, Bacillary

• Prevaccination and postvaccination ELISA measurements of antibody to S sonnei lipopolysaccharide among recipients of S sonnei-rEPA showed that the vaccinees who developed S sonnei shigellosis had significantly lower serum IgG and IgA responses to the homologous lipopolysaccharide than those who did not (p = < 0.05) [28].
• A randomized, double-blind study comparing cefixime and trimethoprim-sulfamethoxazole in the treatment of childhood shigellosis [29].
• Although methylprednisolone therapy induced marked cellular immunosuppression in all four animals, as measured by in vitro assays, no animal had evidence of clinical shigellosis or bacterial shedding [30].
• SETTING: Dhaka Hospital, International Centre for Diarrhoeal Disease Research, Bangladesh. SUBJECTS: 83 children aged 1-7 years with bacteriologically proved shigellosis but no clinical signs of vitamin A deficiency; 42 were randomised to treatment with vitamin A and 41 formed a control group [31].
• We conclude that the dynamics of salivary anti-Shigella LPS and anti-Shiga-toxin in children with dysentery indicate that it can be applied to studies of immune response in shigellosis for epidemiological and vaccination purposes [32].

References