Pediatric Gastroenterology and Infectious Diseases Report (Assessment)

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Microorganisms have evolved to contribute to various infectious diseases in human beings especially by developing an ability to withstand the routine protection offered by the body’s defense mechanisms. One of the pathogens that belong to this category is multidrug-resistant Staphylococcus aureus. Its severe epidemiology was reported to be associated with pandemics for over a decade (Gould, 2007). This has led to a sharp rise in S. aureus bacteraemia with over 50% in many countries (Gould, 2007). In the recent period, this microbe has emerged to cause infections in children worldwide. Research has revealed 446 episodes of community-acquired S. aureus infections and among them, 134 (30%) were caused by MRSA. Here, an increase of 40 % was much confined to children with skin and soft tissue infections indicating that CA-MRSA (community-acquired MRSA) strains might have become endemic within pediatric health care facilities (Zaoutis et al., 2006).

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This pathogen has evolved to withstand potential antibiotics. This is due to the presence of mec A gene present on a mobile genetic element, the Staphylococcal Cassette Chromosome mec (SCCmec) (Deurenberg et al., 2007). There is a total of five different SCC mec types (I-V) and variants of these SCCmec types reported to exist whose genes confer resistance to beta-lactam antibiotics, as well as genes for the regulation of expression of mecA (Deurenberg et al., 2007). However, recent studies have revealed that there were seven main SCCmec types of I to VII (Deurenberg et al., 2009). The mechanisms that contribute to resistance are a mutation of a bacterial gene on the chromosome or transfer of a resistance gene from other organisms by the exchange of genetic information by conjugation, transduction, or transformation (Ito et al., 2003).

The presence of plasmids in Staphylococcus such as 4.5 kb chloramphenicol resistance plasmids, pSK2, and the pSK1 family of multiresistance plasmids, which range in size from 20 to 42 kb was reported to confer resistance to antiseptics and disinfectants, trimethoprim (Tpr), penicillin (Pcr) and the aminoglycosides gentamicin, tobramycin and kanamycin (Gmr Tmr Kmr) (Skurray et al., 1988). Further, the evolution of a multiresistant chromosome in Staph aureus is due to transposition and genetic rearrangement (Skurray et al., 1988). The treatments options for the infections specific to methicillin-resistant Staphylococcus aureus are parenteral antimicrobials such as vancomycin, teicoplanin, daptomycin, linezolid, and tigecycline as they have been proved to be effective in randomized, prospective, double-blind trials (Moellering, 2008).

The other microorganism to be given importance in this part of the description is Pneumococci, more specifically, Streptococcus pneumoniae. It is considered the main agent of community-acquired pneumonia, meningitis, and bacteremia in children including adults (Lynch & Zhanel, 2009). Young children are the prime targets for Invasive pneumococcal disease (IPD) with case fatality rates of less than 3 %. The serotypes of IPD cases are limited in number and show variation in infectivity and virulence (Lynch & Zhanel,2009). In developing countries, especially, alleviating this infectious pathogen seems to be a problematic issue. For example, a report from the UK revealed that it has caused fever and/or suspected invasive bacterial disease in 60 % of children aged <5 years in urban Nepal (Williams et al., 2009).

The mechanisms that contribute to multidrug resistance in Pneumococci are alterations in the structure of six penicillin-binding proteins (PBPs) (1a, 1b, 2x, 2a, 2b and 3) that enable resistance to beta-lactam antibiotics (Reinert ,2009). More particularly, the resistance was reported to be facilitated through the erm (B) gene, which results in macrolide-lincosamide-streptogramin B résistance. Resistance is also acquired through a gene that encodes an antibiotic efflux pump, known as mef (A) gene (Reinert, 2009).

This has strengthened a previous report on the mechanisms of macrolide resistance and clonality in Streptococcus pneumonia (Bozdogan et al. 2004). It was revealed that erm (B) and mef (A) genes were found in 14 of the Streptococcus pneumoniae strains isolated from 24 countries indicating the common distribution of clonal strains across Europe, Asia, and America (Bozdogan et al. 2004). The current treatment options for this pathogen are cephalosporins, carbapenems, glycopeptides, lipopeptides, ketolides, lincosamides, oxazolidinones, glycylcyclines, quinolones, deformylase inhibitors (Van Bambeke et al, 2007.). However, there are certain flaws as they are considered novel with limited action on resistance mechanisms (Van Bambeke et al, 2007).

Vaccination strategies have also emerged to confer protection against pneumococcal infections. Seven-valent pneumococcal conjugate vaccine (PCV7) was reported to contribute to a reduction in nasopharyngeal carriage of penicillin-resistant Streptococcus pneumonia

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(Dagan, 2009). This occurs when the vaccine induces a significant decrease of antibiotic-resistant serotypes. However, penicillin-intermediate serotype 19A was not affected by PCV7 and this has also established the connection between serotype 19A and invasive pneumococcal disease (IPD) in children (Dagan, 2009). Further, investigations may be required to study this controversy.

Next, the contribution of pathogenic microorganisms to infectious diseases continues to exist with Helicobacter pylori in children. This pathogen was reported to cause infections in nearly 50% of the world population where childhood cases constitute the majority. This occurs especially in low socioeconomic conditions where family members run the risk of predisposing their children in early life. The manifestations in children include gastritis, ulcers, mucosal-associated lymphoid type lymphoma, and, rarely, gastric atrophy with/without intestinal metaplasia (ie, both precursor lesions for gastric cancer) (Czinn,2005). Its prevalence in young children after the first year of life was reported to be approximately 30%. This was revealed when a large study on children attending daycare facilities was conducted (Kori, Goldstein & Granot, 2009). Further, the prevalence of H.Pylori infections in association with other complaints has become a problematic issue.

This could be because it is predisposing Iranian children to recurrent abdominal pain (RAP) who are in the age range of 12-13, (Masoodpoor, Darakhshan & Sheikhvatan, 2009). Similarly, the epidemiology of H.pylori was reported to be high in children who are refugees in Western Australia (Cherian et al., 2008). These examples better strengthen the prevalence and epidemiology of H.pylori infections in children. It was described that H pylori infection shows variation between countries and within countries in addition to ethnic and racial factors, socio-economic status and living conditions that affect the prevalence of infection (Mittal & Mathew, 2003). This trend could more likely affect developing countries where the prevalence of infection is very high (Mittal & Mathew, 2003).

This could be better evidenced by a study where genotype changes among different ethnic groups in Thailand were reported to contribute to the incidence of H.pylori infections. (Vilaichone, 2004). The studied individuals were those of ethnic Thai, ethnic Chinese and Thai-Chinese being classified as were categorized into East Asian, South/Central Asian, Western or mixed types. The genotype was described to be the most common among Chinese (85%) and Thai-Chinese (55%) was East Asian. This study has indicated the genotype changes of H.pylori from East Asian to South Asian (Vilaichone, 2004).

H.pylori infections in children are also showing changes from an underdeveloped to a developed country which could be attributed to differences in socioeconomic status, sanitation, and household hygiene (Tkachenko et al., 2007). This was revealed when 2 cross-sectional studies were conducted among children in St Petersburg, Russia (Tkachenko et al., 2007). This has strengthened an earlier report that described the changes in the prevalence of H. pylori due to differences between the communities in the incidence (Pounder, 1995). As such, two groups of countries were identified in this context where one group has the majority of children with H.pylori infections and second group where only a few children are reported to be infected but with the continuity of infection till the adult stage (Pounder, 1995).

The other disease of much research attention is Coeliac disease, which is a severe autoimmune disorder of gastrointestinal origin most prevalent in children with increased genetic predisposition. Here, serum autoantibodies were considered for the detection of celiac disease; especially serum tissue transglutaminase and endomysial autoantibodies indicate small-bowel abnormalities indicative of celiac disease (Markku Mäki et al.). Its prevalence was reported to be rare among African-Caribbean, Japanese and Chinese backgrounds and also in India (Ajit Sood et al., 2006). This was revealed when a study on 4347 school children was conducted in North India that indicated the presence of antitissue transglutaminase antibodies (Ajit Sood et al., 2006). This could indicate the importance of sociodemographic data in understanding the prevalence rates of coeliac disease. Hence, trends in the variation of sociodemographic factors have received paramount importance with regard to the clinical characteristics of celiac disease in children (Ajit Sood et al., 2006).

Further, the high prevalence of coeliac disease was associated with the idiopathic short stature (ISS), as described in a study, by measuring serologic markers like immunoglobulin (Ig) A G antigliadin antibodies (AGA) and transglutaminase (TTG) antibodies for CD and performing an intestinal biopsy (Hashemi et al., 2008). The change in the incidence of this disease was the difference in the prevalence rates among different countries. A study described that polish children were moderately acquiring the infections by developing asymptomatic or oligosymptomatic courses when compared to other countries (Szaflarska-Popławska et al., 2009).

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Similarly, a report from Sweden described regional variation in celiac disease when countrywide analysis on incidence was made from 1998 to 2003(Olsson et al., 2009). This was reported to be associated with multifactorial disease etiology (Olsson et al., 2009). In contrast, the prevalence of celiac disease in different countries in the Middle East, North Africa, and India was reported to be the same as that in Western countries. Hence, patients with chronic diarrhoea or iron deficiency anaemia could be considered suspicious for coeliac disease in developing countries (Malekzadeh, Sachdev & Fahid Ali).

Next, children susceptible to yet another prevalent disease is Biliary atresia. It involves the destruction of the bile duct outside the liver mostly and the symptoms typically get manifested in children. Different tests are required to confirm the pathology of Biliary atresia like blood tests, urine tests, ultrasound scan of the liver, tests to visualize the flow of bile through the liver and liver biopsy.

This disorder often involves a defect in the levels of bile salts in the intestine that are required for fat digestion, accompanied by poor growth and deficiency of fat-soluble vitamins like A, D, E and K. This may indicate an association between Biliary atresia and failure to thrive condition.

Investigations have revealed that Liver transplantation is common for patients with Biliary atresia in addition to Kasai portoenterostomy operation (Middlesworth & Altman, 1997). The kasai procedure is based on connecting the liver directly to the small intestine with a loop of the small intestine. This facilitates the flow from the small bile ducts inside the liver straight into the intestine. A failure to thrive or hypocholesterolemia was also anticipated in children with Biliary atresia when the liver transplantation is performed late (Hasegawa et al, 1997). Children with Biliary atresia run short of essential nutrients like vitamins A, D, E and the trace elements like zinc and copper. This defect could be better assessed by measuring the serum levels of these vitamins. This nutrition intervention also sets the patients to mentally face the recommended liver transplantation therapy (Cywes & Millar, 1990). Similarly, children with Biliary atresia were reported to have abnormalities of amino acids like isoleucine, leucine, and valine, phenylalanine and tyrosine (Weisdorf et al, 1987). This defect could be better assessed by measuring the plasma levels of these amino acids. Hence the nutrition deficiencies in children with Biliary Atresia could be better managed by improving the children’s diet with essential vitamins and manipulation of the amino acid distribution in dietary protein (Weisdorf et al, 1987).

References

Ajit Sood, Vandana Midha, Neena Sood, Gurcharan Avasthi, Alok Sehgal. “Prevalence of Celiac Disease Among School Children in Punjab, North India.” J Gastroenterol Hepatol.21 (2006):1622-1625.

27. Biliary Atresia.

Bozdogan, B, Bogdanovich, T, Kosowska, K, Jacobs, MR, Appelbaum, PC.” Macrolide resistance in Streptococcus pneumoniae: clonality and mechanisms of resistance in 24 countries.” Curr Drug Targets Infect Disord 4(2004); 169-76.

Cherian, S, Forbes, D, Sanfilippo, F, Cook, A, Burgner, D. “The epidemiology of Helicobacter pylori infection in African refugee children resettled in Australia.” Med J 8(2008):438-41.

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Cywes, C & Millar, AJ. “Assessment of the nutritional status of infants and children with biliary atresia.” S Afr Med J.77(1990):131-5.

Czinn, SJ. (2005). “Helicobacter pylori infection: detection, investigation, and management.” J Pediatr 146(2005):S21-6.

Dagan, R.“Impact of pneumococcal conjugate vaccine on infections caused by antibiotic- resistant Streptococcus pneumoniae.” Clin Microbiol Infect 15(2009):16-20.

Deurenberg RH, Vink C, Colonic S, Friedrich AW, Bruggeman CA, Stobberingh EE. “The molecular evolution of methicillin-resistant Staphylococcus aureus.” Clin Microbiol Infect 13(2007):222-35

Deurenberg, RH, Stobberingh, EE. “The molecular evolution of hospital- and community- associated methicillin-resistant Staphylococcus aureus.” Curr Mol Med 9(2009):100-15.

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Hasegawa, T, Fukui, Y, Tanano, H, Kobayashi, T, Fukuzawa, M, Okada A. “Factors influencing the outcome of liver transplantation for biliary atresia.” J Pediatr Surg 32(1997):1548-51.

Hashemi, J, Hajiani, E, Shahbazin, HB, Masjedizadeh, R, Ghasemi, N. “Prevalence of celiac disease in Iranian children with idiopathic short stature.” World J Gastroenterol. 14(2008):7376-80.

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Kori, M, Goldstein, E, Granot, E. “Helicobacter pylori infection in young children detected by a monoclonal stool antigen immunoassay.” Pediatr Infect Dis J. 28(2009):157-9.

Lynch, JP 3rd & Zhanel GG. “Streptococcus pneumoniae: epidemiology, risk factors, and strategies for prevention.” Semin Respir Crit Care Med 30(2009): 189-209.

Malekzadeh R, Sachdev A, Fahid Ali A. “Coeliac disease in developing countries: Middle East, India and North Africa.”Best Pract Res Clin Gastroenterol. 19(2005):351-8.

Markku Mäki, Kirsi Mustalahti, Jorma Kokkonen, Petri Kulmala, Mila Haapalahti, Tuomo Karttunen, Jorma Ilonen, Kaija Laurila, Ingrid Dahlbom, Tony Hansson, Peter Höpfl, Mikael Knip. Prevalence of Celiac Disease among Children in Finland.

Masoodpoor, N, Darakhshan, Sheikhvatan, M. “Helicobacter pylori infection in Iranian children with recurrent abdominal pain.” Trop Gastroenterol 29(2008):221-3.

Mittal, SK & Mathew, JL. Helicobacter pylori infection in children: a review. Trop Gastroenterol 24(2003):106-15.

Middlesworth, W & Altman, RP. “Biliary atresia.” Curr Opin Pediatr 9(1997):265-9.

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Szaflarska-Popławska A, Parzecka M, Müller L, Placek W. “Screening for celiac disease in Poland.” Med Sci Monit. 15(2009):PH7-11

Tkachenko, MA, Zhannat, NZ, Erman, LV, Blashenkova, EL, Isachenko, SV, Isachenko, OB, Graham, DY, Malaty, HM. “Dramatic changes in the prevalence of Helicobacter pylori infection during childhood: a 10-year follow-up study in Russia.” J Pediatr Gastroenterol Nutr. 45(2007):428-32

Van Bambeke, F, Reinert, RR, Appelbaum, PC, Tulkens, PM, Peetermans, WE. “Multidrug-resistant Streptococcus pneumoniae infections: current and future therapeutic options.” Drugs 67(2007):2355-82.

Weisdorf, SA, Freese, DK, Fath, JJ, Tsai, MY, Cerra, FB. “Amino acid abnormalities in infants with extrahepatic biliary atresia and cirrhosis.” J Pediatr Gastroenterol Nutr 6(1987):860-4

Williams EJ, Thorson S, Maskey M, Mahat S, Hamaluba M, Dongol S, Werno AM, Yadav BK, Shah AS, Kelly DF, Adhikari N, Pollard AJ, Murdoch DR. “Hospital-based surveillance of invasive pneumococcal disease among young children in urban Nepal.” Clin Infect Dis 48 (2009):s114-22.

Zaoutis TE, Toltzis P, Chu J, Abrams T, Dul M, Kim J, McGowan KL, Coffin SE. “Clinical and molecular epidemiology of community-acquired methicillin-resistant Staphylococcus aureus infections among children with risk factors for health care-associated infection: 2001-2003.” Pediatr Infect Dis J 25 (2006):343-8.

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IvyPanda. 2022. "Pediatric Gastroenterology and Infectious Diseases." August 22, 2022. https://ivypanda.com/essays/pediatric-gastroenterology-and-infectious-diseases/.

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