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The incubation period of C. diphtheriae is between 2-5 days meaning that symptoms will not appear immediately after infection. Initially, a sore throat, fever, nasal discharge, and swollen lymph nodes in the neck will develop. Following this, a thick, gray coating, or pseudomembrane, will grow on the back of the throat making it difficult to swallow and breathe. The pseudomembrane is a congregation of dead tissue that was caused by the diphtheria toxin. If left untreated, this can cause long-lasting respiratory complications. Also, if the toxin is in circulation for long periods of time, it can permanently damage certain tissues of the body. For example, it can target heart tissue and lead to myocarditis or it can damage the nerve tissues, especially in the neck, and cause swallowing complications indefinitely [10] . C. diphtheriae can also colonize the skin when an open cut is exposed to it. The lesion will display common symptoms of all bacterial skin infections including redness, swelling, and pain in the region. Also, gray tissues from resulting from dead tissue can surround the laceration [11] .

Early diagnosis of this disease is very important because delayed treatment could possibly result in death. Diphtheria can often be confused with other illnesses, so a proper diagnosis in a laboratory is necessary. It is ideal to culture a specimen obtained from the infected patient on blood agar and selective tellurite media. C. diphtheriae reduce the tellurite salts, which result in the development of black colonies on the media making diagnosis of this disease accurate and clear [12] .

Often, treatment is administered to an infected patient before getting the diagnostic results from a laboratory to increase the chances of complete eradication of the disease. Antitoxin and antibiotics are the main and most effective form of treatment for diphtheria. The antitoxin, which is extracted from horses, targets and neutralizes the DT found throughout the bloodstream to stop the progression of the illness. It is not able to inhibit DT that is already bound to tissues, however. The next common form of treatment is the administration of erythromycin or penicillin, which also targets the toxin and stops the growth of the bacteria. These forms of treatment are both effective in preventing the transmission of diphtheria to other susceptible hosts [10] .

There are four vaccines that have been developed to treat diphtheria: DTaP, DT, Td, and Tdap. They were formulated as a combination with other drugs to also treat tetanus and pertussis. DTaP and DT are given to children under the age of seven, while Td and Tdap are administered during adolescence or adulthood. The latter two vaccines are used as boosters and are not given at the same time Burberry DK88 top handle bag Discount Very Cheap Discount Geniue Stockist Limited Free Shipping New Free Shipping Fast Delivery AYaEp

Receiving the full round of vaccinations for diphtheria is the most effective preventative measure one can take. However, if someone does contract the disease, it is necessary to prevent the transmissions of the disease to others. Isolation of those carrying the disease until they have received a clearing by a medical professional is the best way to prevent the spread of diphtheria. Also, those who come into contact with the bacteria, but aren’t showing any symptoms should also receive medicinal treatment to prevent any possible transmission [14] .

We investigated the ability of the wild-type strain 52145R and its derived unencapsulated mutant 52K0 to attach to and invade human lung epithelial cells (Fig. 1 ). The unencapsulated mutant 52K0 attached to and invaded epithelial cells with high efficiency compared to the wild-type strain 52145R. The unencapsulated mutant showed approximately 10-fold-greater efficiency of adhesion and internalization than the wild-type strain. These results confirm that CPS modulates the interactions between K. pneumoniae and human lung epithelial cells.

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FIG. 1.

Adhesion (A) and internalization (B) of wild-type strain 52145R and its derived isogenic unencapsulated mutant 52K0 by human lung epithelial cells. The results are expressed in CFU per monolayer. The data are the mean plus standard deviation of at least three independent experiments ( < 0.01 for comparison between the unencapsulated mutant and the encapsulated wild-type strain for the adhesion and internalization experiments; two-tailed test). (C) Transmission electron micrograph of an A549 human lung epithelial cell infected by the unencapsulated strain 52K0. The arrows indicate three bacterial cells surrounded by vacuolar membranes. (D) Transmission electron micrograph of a lung section from a mouse infected with the unencapsulated strain 52K0. The arrow indicates a bacterial cell adhering to lung epithelial cells.

We studied recovery over time of the intracellular wild-type strain 52145R and the unencapsulated mutant 52K0 from infected lung epithelial cells. After 6 h of incubation, the number of viable bacteria had decreased to 50% of the intracellular bacteria recovered after 2 h of incubation (Fig. 2 ). Viable intracellular bacteria continued to decline over time, and after 24 h, only 8% of the bacteria recovered after 2 h of incubation were viable. Reduction of bacterial viability over time was not due to the exposure of the cells to gentamicin, since we obtained identical results in parallel experiments without gentamicin. After 24 h of incubation, we determined the viability of the epithelial cells by measuring the number of cells that failed to exclude trypan blue. More than 80% of the epithelial cells remained viable, suggesting that epithelial cell death accounted for some, but not all, of the decline in the number of intracellular bacteria. Thus, intracellular bacteria, both the wild-type strain and the unencapsulated mutant, were not able to multiply in the epithelial cells, and after 24 h of incubation, 92% of the bacteria were nonviable.

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FIG. 2.

Survival of within human lung epithelial cells. After inoculation of A549 cells with strain 52145R (open circles) and 52K0 (solid circles), the cells were incubated in the presence of gentamicin for various periods and then washed and lysed for quantitative culture. The data are the mean ± standard deviation of at least three independent experiments.

Role of K. pneumoniae entry into lung epithelial cells. The results described above present an apparent paradox: reduction of capsule expression increased adhesion to and invasion of human lung epithelial cells. However, clinical and experimental observations suggest that encapsulated strains are more virulent than unencapsulated strains. If adhesion to and invasion of lung epithelial cells were a virulence mechanism for lower respiratory tract infections, we would expect that unencapsulated strains would be virulent in an animal model of pneumonia. In contrast, if the entry of K. pneumoniae into epithelial cells were not a virulence mechanism but rather represented a mechanism to contain the infection, unencapsulated strains would be expected to exhibit reduced virulence.

This work is the first to investigate factors that may predispose developing world children with no known gastrointestinal pathology to SIBO. The significance of growth stunting in our model demonstrates an association between linear growth delay and overgrowth independent of diarrheal disease and sanitation. However, in the absence of longitudinal analysis, the details of this association remain unclear. Given the known nutritional consequences of SIBO in other settings, it is biologically plausible that SIBO plays a causative role in growth stunting. It is also possible that a variable we did not measure in our analysis leads to both SIBO and declining LAZ and thus is acting as a confounder in our model.

We designed our regression model to investigate two competing hypotheses on why children would develop SIBO from their environment. The first hypothesis was that children develop SIBO due to lumenal stasis secondary to gastroparesis or ileus after recent or recurrent enteric infection. This is biologically plausible given that children in Bangladesh have a mean of 4.7 diarrheal episodes and a median of 3.3 enteric pathogens identified in nondiarrheal stools in the first year of life alone ( 42 ). The second hypothesis that has been suggested is that children develop a functional motility disorder with a hypoactive migrating motor complex and decreased intestinal contractility due to constant lipopolysaccharide exposure from an unsanitary environment ( 43 ). This phenomenon has been shown to occur in animal models and in women with late radiation enteropathy ( 44 46 ). Our analysis suggests that recent or frequent enteric infection does not predispose to SIBO, while measures of environmental contamination do. Although we did not test motility in this study, our results suggest this endeavor might be fruitful in future investigation.

To date, literature on environmentally derived SIBO in the developing world is sparse. It has been shown that SIBO occurs in the lower socioeconomic strata of developing world countries with increased prevalence compared to countries with greater financial means ( 2018 New For Sale Free Shipping Sast Chloé contrast trim jumper qSfbDiitm
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). SIBO in this setting has been shown to lead to poor carbohydrate absorption and oral vaccine underperformance ( 32 Cheap Manchester Great Sale Best Sale Cheap Online Isabel Marant Pretley leather trousers Free Shipping Pick A Best Clearance Best Seller xIzQv
34 ). It has also been shown to have increased prevalence in severe malnutrition ( 47 ). Much of our understanding of the pathogenesis of SIBO comes from studies in the developed world in patients with underlying gastrointestinal pathology. While these studies are extremely informative, it is important to understand that the pathogenesis and pathophysiology of SIBO in developing world children with no underlying gastrointestinal disease may be different from those of patients in industrialized countries.