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14nia and is accompanied by the development of bronchial obstruction. In contrast to atypical pneumonia, pneumococcal pneumonia is characterized by more pronounced inflammatory changes in the complete blood count, such as leukocytosis, neutrophilia, and an accelerated ESR. The most common morphologic form of pneumococcal pneumonia is focal and focal-fluid, and mycoplasma and chlamydial pneumonia is focal.
References:
1. Diagnostic significance of clinical and para-clinical signs of community-acquired pneumonia in children. 2020.
2. Koloskova, O. K., Tarnavska, S. I., Shakhova, O. O., & Prunchak, N. I. Features of the course of uncomplicated community-acquired pneumonia in children with regard to leukocyte blood indices.
3. Farnaes, L., Wilke, J., Loker, K. R., Bradley, J. S., Cannavino, C. R., Hong, D. K., ... & Coufal, N. G. (2019). Community-acquired pneumonia in children: cell-free plasma sequencing for diagnosis and management. Diagnostic microbiology and infectious disease, 94(2), 188-191
4. Gonchar, M. O., Senatorova, G. S., Telnova, L. G., & Omelchenko, O. V. (2020). Differential diagnosis of dyspnea syndrome. Pneumonia in children. Complications of pneumonia. Emergency care in acute respiratory failure in children: guidelines.
5. Frolova, T. V., Borodina, O. S., Tereshchen-kova, I. I., Stenkova, N. F., & Sinyayeva, I. R. (2019).
The course of community-acquired uncomplicated pneumonia in children with different levels of physical development.
6. Pasik, V. Y. (2020). Features of the clinical course of community-acquired pneumonia in young children. Ukrainian Journal of Perinatology and Pediatrics, (3 (83)), 59-65.
7. Koval, L. I., Kravchenko, T. Y., Lotysh, N. G., & Papinko, R. M. (2019). Community-acquired pneumonia in children: energy metabolism disorders and individual genetic polymorphism.
8. Yun, K. W., Wallihan, R., Juergensen, A., Mejias, A., & Ramilo, O. (2019). Community-acquired pneumonia in children: myths and facts. American journal of perinatology, 36(S 02), S54-S57.
9. Nechytailo, Y. M., Popeliuk, N. O., Dolzhenko, O. G., Nechytailo, Y. N., & Popeliuk, N. A. (2021). Pharmacoeconomic features of inpatient treatment of acute community-acquired pneumonia in children.
10. Nascimento-Carvalho, C. M. (2020). Community-acquired pneumonia among children: the latest evidence for an updated management. Jornal de pediatria, 96, 29-38.
11. Shcherbatyuk, N., Gariyan, T., Mudryk, U., Chornomydz, I., & Horishnyi, I. (2023). Effect of antibiotics of different groups on the course of community-acquired pneumonia in children. Journal of Medical and Biological Research, (1), 22-25.
UDC: 616.36-002-02-036.22-07-08-084
Melenko Svitlana Romanivna,
PhD, Associate Professor of the Department of Infectious Diseases and Epidemiology
Bukovinian State Medical University Skrypnyk Valentyna Valentynivna,
student
Bukovinian State Medical University Glukhova Anna Yosifivna,
student
Bukovinian State Medical University DOI: 10.24412/2520-6990-2023-9168-64-68 VIRAL HEPATITIS D: ETIOLOGY, EPIDEMIOLOGY, PATHOGENESIS, CLINIC, TREATMENT,
DIAGNOSIS AND PREVENTION
Abstract.
Today, chronic hepatitis is one of the most important problems in modern gastroenterology. Every year, more than 1 million people die from chronic liver disease and its complications. Timely diagnosis, treatment and prevention can prevent the progression of the disease, the development of complications, liver fibrosis and cirrhosis and, accordingly, reduce the percentage of fatalities.
Hepatitis D is the most severe form of viral hepatitis with rapid progression to cirrhosis, increased risk of hepatocellular carcinoma and mortality compared to hepatitis B monoinfection.
Key words.: Hepatitis D, relevance, prevention.
Etiology.
Hepatitis D virus (HDV) occupies an intermediate position between viruses and viroids. HDV is a small (35-37 nm in diameter) RNA-containing virus discovered in 1977 [ 5 , 17 ] .It does not have its own outer envelope. HDV contains a nucleus with a single-stranded RNA of negative polarity. The virion is defective because it requires the hepatitis B surface antigen (HBsAg) for infection [ 18 ]. The outer
envelope is composed of HBsAg of the hepatitis B virus. Therefore, HDV cannot exist without HBV, because it needs it as a source of HBsAg. HBsAg serves as a coat protein, allowing HDV to enter hepatocytes [19]. Both HBV and HDV bind to heparan sulfate proteoglycans for adsorption to hepatocytes [20] and use the sodium taurocholate cotransporter polypeptide receptor to enter cells [19].
Hepatitis D virus RNA is a small genome consisting of 1700 nucleotides [7]. There are two hepatitis delta antigens (HDAg): small HDAg (24 kDa) and large HDAg (27 kDa), which is 214 amino acids long. Small HDAg accelerates genome synthesis, while large HDAg inhibits HDV RNA synthesis but is required for virion morphogenesis [7].
Eight different genotypes of IOP have been identified [15,21]. The geographical distribution of IOP genotypes has changed over time, most likely due to human migration. Currently, genotype 1 is the most common and predominant genotype in Europe and North America. Genotype 2 was previously restricted to Asia, but has now appeared in the Middle East, including Iran and Egypt. Genotype 3 is mainly found in the Amazon basin in South America. Genotype 4 is mainly found in Taiwan, China and Japan. Meanwhile, genotypes 5, 6, 7 and 8 have traditionally been found only in Africa, but recent reports describe the migration of genotypes 5, 6 and 7 to different parts of Europe. However, Central Africa is considered to be the main site of IHD diversification with the presence of genotypes 1, 5, 6, 7 and 8. It is well known that the specificity of the IHD genotype affects clinical outcomes. Genotype 3 of IHD is the most pathogenic of all IHD genotypes. It has been shown that patients with genotype 1 of IHD have lower remission rates, more aggressive disease and worse outcomes than patients with genotype 2 of IHD [6,15,16].
The core of HDV is an HD-Ag of protein nature. HDV is resistant to high temperatures, acids, UV light, but sensitive to alkalis. . Repeated freezing and reflow do not affect its activity [7].
Epidemiology.
IHD is described as the most severe form of viral hepatitis with progression to cirrhosis in 10-15% of patients within 2 years and in 70-80% of patients within 5-10 years [6].It is estimated that hepatitis delta virus (HDV) coinfection occurs in approximately 5-10.6% of patients with chronic hepatitis B virus (HBV) infection, affecting up to 72 million people worldwide [1-4]. The prevalence of HDV infection is believed to be increasing in many parts of the world due to increased injecting drug use, sexual transmission, and immigration from high endemic areas [3, 5-8,12].
The main source of infection is patients with acute or chronic hepatitis D. The mechanism of transmission is hemocontact, and the main route of transmission is parenteral, mainly through the blood [9]. People who have not had hepatitis B and people with chronic HBV infection are susceptible to HDV. The risk of infection is especially high in regular recipients of donated blood and its products (haemophiliacs), frequently ill people receiving parenteral treatment, injecting drug users, etc. Transplacental transmission is possible, especially in HBe-positive mothers infected with HDV. Perinatal transmission is rare, but the development of HBV and HDV coinfection in newborns is possible. Sexual transmission is also possible. People who are immune to hepatitis B (anti-HBs are detected in the blood) are not susceptible to HDV [18].
Pathogenesis.
The development of the pathological process in hepatitis D is possible only in the presence of HBV. Infection with HDV occurs simultaneously (or together) with HBV.
There are two possible ways of getting infected:
- Co-infection - when a healthy person becomes infected.
- Superinfection - when a person with acute hepatitis B or chronic HBV infection becomes infected.
From the blood, HDV enters hepatocytes and localises in the nucleus. Here, HDV RNA replicates in the hepatocyte cytoplasm and HBsAg is synthesised. As a result, new HDV virions are formed, which infect healthy hepatocytes. HDV also inhibits HBV replication by using HBsAg[6,13].
If it is a coinfection, then the plastic material (HBsAg) is exhausted over a certain period of time and the formation of new HDV virions stops. In case of coinfection, hepatitis D in most cases has an acute course with a high probability of HDV elimination from the body and recovery[13].
If it is a superinfection, then large amounts of HBsAg are constantly produced in the liver cells. As a result, a fairly large number of new HDVs are formed. With a pronounced cytopathic effect, HDV causes severe liver damage with possible parenchymal necrosis. In case of superinfection, hepatitis D has a severe course with frequent development of fulminant forms of the disease. In the case of chronic hepatitis D, the pathological process is highly active and cirrhosis occurs very quickly. There is no immune response to HD. Antibodies to HDV appear late. IgM on the 1st-15th day of the disease, IgG on the 5th-9th week [13].
Clinical picture and typical course of the disease:
Simultaneous acute infection with hepatitis B and hepatitis D (coinfection) is known as hepatitis B. Therefore, the symptoms of hepatitis D are similar to those of hepatitis B:
- yellowing of the skin and eye sclera (jaundice);
- darkening of urine;
- discoloured faeces;
- digestive disorders;
- pain in the liver (in the right hypochondrium);
- nausea, vomiting;
- increased fatigue;
- loss of appetite;
- arthralgia (joint pain);
- fever (prolonged increase in body temperature);
- skin rashes.
These signs usually appear 3-7 weeks after the initial infection [28,31].
HDV (hepatitis D) superinfection accelerates the development of cirrhosis - it develops almost 10 years earlier compared to patients with chronic HBV (hepatitis B virus) monoinfection, despite the fact that HDV inhibits HBV replication [23,35].
Chronic HBV is defined as the presence of infection for more than 6 months. The clinical course of the disease may be asymptomatic, and patients may present with nonspecific symptoms of fatigue, malaise and anorexia [32,22]. Three distinct chronic HB V/HCV types have been described. Most patients will have
predominantly HBV replication with suppressed HBV replication and negative HBeAg levels. A similar phenomenon is also observed in hepatitis C and D virus infected patients, in which the hepatitis D virus suppresses hepatitis C virus replication[25,30].
The period of remission of chronic hepatitis D:
1. No complaints. Signs of the disease are detected only by the results of histological examination of liver biopsies - a 2-fold decrease in the histological activity index and the absence of further fibrosis;
2. Absence of replication markers (HBeAg, HDV DNA, anti-HDcor IgM) for 6 months;
3. AlAt and AsAt levels are normal [38,26].
Diagnosis of viral hepatitis D:
Diagnosis and treatment of acute hepatitis B and D is performed by an infectious disease specialist, and chronic hepatitis by a hepatologist or gastroenterologist. The diagnosis is made on the basis of the clinic, medical history, and laboratory tests [24, 27].
The main method of diagnosis of hepatitis D virus is the detection of high titres of immunoglobulin G (IgG) and immunoglobulin M (IgM) to HDV, and is confirmed by detection of HDV RNA in the serum by polymerase chain reaction (PCR). IgM persists for about 6 weeks (exceptionally, 12), after which it is replaced by IgG antibodies. HBsAg is detected in low titres or is undetectable (suppression by hepatitis D virus, often also true for IgM anti-HBc antibodies) [29,33]. In superinfections, IgM anti-HDV antibodies are present, which are later replaced by IgG. If chronic HDV infection is associated with active hepatitis, then anti-HDV IgM antibodies persist in the blood. People who have been cured of HDV infection retain IgG antibodies.
The necessary research methods include general clinical tests (complete blood count, urinalysis, biochemical analysis, coagulogram) to determine the degree of liver damage and identify complications. There is an increase in ESR with high activity of the inflammatory process; dysproteinemia with moderate and high activity of the CHB; increased ALT, AST, GGT, ALP, total bilirubin and its fractions, total cholesterol in cholestasis syndrome, thymol test; decreased T-lymphocytes, increased levels of immunoglobulins, circulating immune complexes, mainly with high and moderate activity of the process [36,37].
Ultrasound examination of the liver is also performed, which shows compaction of the liver parenchyma, intrahepatic bile ducts and liver vessel walls; radioisotope studies (bilyscintigraphy) - a decrease in the hepatic capture index, the percentage of accumulated RFP, a decrease in the retention rate of RFP in the blood; conjunctival biomicroscopy - the presence of vascular, intravascular, extravascular disorders that correspond to the degree of liver damage. Liver biopsy - performed to determine the progression of the disease [34].
Basic principles of treatment:
- proper, balanced nutrition;
- limiting medication intake;
- elimination of factors that can provoke exacerbations (insolation, frequent respiratory diseases, contact with toxic substances);
- drug therapy:
1. alpha-interferons (Intron A, Laferon, etc.) - 5-6 MMU/sq.m 3 times a week for 6-12 months or lamivudine (for children from 3 months to 12 years - 3 mg/kg body weight 2 times a day, but not more than 100 mg/day).
2. Sorbents (enterosgel, otonil, etc. for 7 days) in age-appropriate doses;
3. Antioxidants - ayevit, unithiol 5% solution at the rate of 5 mg/kg body weight for 10-14 days twice a year (D).
4. Dufalac (lactulose)
5. Hepatoprotectors and drugs that improve bile secretion (Antral, Milk Thistle, Carsil, Glutargin, Essentiale, Darcil)
6. Prebiotics, probiotics (according to indications, 3 weeks - 3-4 times a year).
The goal of treatment is complete eradication of HDV, elimination of the active inflammatory process in the liver, and prevention of progression and development of complications[24].
Differential diagnosis is carried out with the following diseases:
- exacerbation of chronic hepatitis;
- toxic liver damage (drug, alcohol);
- cirrhosis of the liver;
- autoimmune hepatitis;
- non-alcoholic steatohepatitis;
- acute liver ischaemia [33].
Prevention of the spread of hepatitis D:
A specific method of preventing hepatitis D is vaccination against hepatitis B.
Nonspecific prevention methods include:
- use of sterile instruments during cosmetic procedures;
- compliance with the rules of asepsis and antisepsis in medical institutions;
- compliance with personal hygiene rules;
- use of barrier methods of contraception during sexual intercourse;
- refusal from drugs;
- avoiding casual sex;
- use of sterile injection equipment [37].
In case of untimely and improper treatment, a number of complications arise: liver cirrhosis, liver cancer, hepatic coma, biliary tract pathology, and death.
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2. Hughes SA, Wedemeyer H, Harrison PM. Hepatitis delta virus. Lancet 2011; 378(9785): 73-85.
3. Rizzetto M Hepatitis D: Thirty years after. Journal of Hepatology 2009; 50(5): 1043-50.
4. Chen HY, Shen DT, Ji DZ, et al. Prevalence and burden of hepatitis D virus infection in the global population: a systematic review and meta-analysis. Gut 2018; 68: 512-21. •• This systematic review and meta-analysis found that the prevalence of HDV among HBsAg-positive individuals may be higher than was previously reported.
5. Rizzetto M Hepatitis D virus: introduction and epidemiology. Cold Spring Harb Perspect Med 2015; 5(7): a021576.
24. Rizzetto M, Canese MG, Aricó S, et al. Immunofluorescence detection of new antigen-antibody system (delta/anti-delta) associated to hepatitis B virus in liver and in serum of HBsAg carriers. Gut 1977; 18(12): 997-1003.
6. Da B.L., Heller Th., Koh Ch. (2019) Hepatitis D infection: from initial discovery to current investiga-tional therapies. Gastroenterology Report, June 23, goz023.
7.Taylor JM. Hepatitis delta virus. Virology 2006; 344: 71- 6.
8. Cross TJ, Rizzi P, Horner M, et a
9. Rizzetto M, Ciancio A. 2012. Epidemiology of hepatitis D. Semin Liver Dis 32: 211-219.
10. Baig S, Siddiqui AA, Ahmed WU, Qureshi H, Arif A. 2009. Frequency of hepatitis C and D super infection in patients with hepatitis B related complex liver disorders. J Coll Physicians Surg Pak 19: 699703.
11. Shaikh MA, Shaikh WM, Solangi GA, Shaikh BA, Soomro MA. 2011. Frequency of hepatitis D virus infection in hepatitis B surface antigen-positive liver diseases. J Coll Physicians Surg Pak 21: 23-25.
12. Soriano V, Grint D, d'Arminio Monforte A, Horban A, Leen C, Poveda E, Antunes F, de Wit S, Lundgren J, Rockstroh J, et al. 2011. Hepatitis delta in HIV-infected individuals in Europe. AIDS 25: 19871992.
13. Taylor JM. 2015. Hepatitis D virus replication. Cold Spring Harb Perspect Med 10.1101/cshper-spect.a021568.
14. Wedemeyer H, Manns MP. 2010. Epidemiology, pathogenesis and management of hepatitis D: Update and challenges ahead. Nat Rev Gastroenterol Hepatol 7: 31-40.
15. Su CW, Huang YH, Huo TI, et al. Genotypes and viremia of hepatitis B and D viruses are associated with outcomes of chronic hepatitis D patients. Gastroenterology 2006; 130(6): 1625-35.
16. Casey JL, Niro GA, Engle RE, et al. Hepatitis B virus (HBV)/hepatitis D virus (HDV) coinfection in outbreaks of acute hepatitis in the Peruvian Amazon basin: the roles of HDV genotype III and HBV genotype F. J Infect Dis 1996; 174(5): 920-6.
17.Rizzetto M, Canese MG, Aricó S, et al. Immunofluorescence detection of new antigen-antibody system (delta/anti-delta) associated to hepatitis B virus in liver and in serum of HBsAg carriers. Gut 1977; 18(12): 997-1003.
18. Grabowski J, Wedemeyer H. Hepatitis delta: immunopathogenesis and clinical challenges. Dig Dis 2010; 28(1): 133-8.
19. He W, Ren B, Mao F, et al. Hepatitis D virus infection of mice expressing human sodium taurocho-late co-transporting polypeptide. PLoS Pathog 2015; 11(4): e1004840.
20. Verrier ER, Colpitts CC, Bach C, et al. A targeted functional RNA interference screen uncovers glypican 5 as an entry factor for hepatitis B and D viruses. Hepatology 2016; 63(1): 35-48.
21. Rizzetto M, Canese MG, Arico S, et al. Immunofluorescence detection of new antigen-antibody system (delta/anti-delta) associated to hepatitis B virus in liver and in serum of HBsAg carriers. Gut 1977; 18(12): 997-1003.
22. International statistical classification of diseases and relatives of health care problems, 10th revision. - World organization of health care., 1998. - 685 p.
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28. Gubergryts N.B. Chronic hepatitis and liver cirrhosis. Contemporary classification, diagnosis and treatment / Educational allowance for interns and doctors, LLC "Lebed", Donetsk. - 2002. - 166 p.
29. Schalm SW, Heathcote J, Cianciara J, Farrell G. et al. Lamivudine and alfa interferon combination treatment of patients with chronic hepatitis B infection: a randomized trial. Gut 2000; 46: P. 562-8.
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35. Flink HJ, van Zonneveld M, Hasen BE, de Man RA, Schalm SW, Janssen HL. Treatment with Peg-interferon alfa-2a for HBeAg-positive chronic hepatitis B: HbsAg Loss is Assotiated with HBV Genotipe, Am. J. Gastroenterol, 2006; 101 (2). - P. 297303.
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UDC: 616.931-036.22-07
HBeAg-negative chronic hepatitis B in the UK. Presented at the ISPOR meeting, May 15-18 2005. Washington DC.
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Melenko Svitlana Romanivna
PhD, Associate Professor of the Department of Infectious Diseases and Epidemiology
Bukovinian State Medical University Zahoruiko Veronika Yuriivna student
Bukovinian State Medical University Chorna Liydmyla Ivanivna
student
Bukovinian State Medical University DOI: 10.24412/2520-6990-2023-9168-68-69 DIPHTHERIA AND ITS CHANGING EPIDEMIOLOGY
Abstract:
In 1999, in an article published in La Revue de Médecine Interne, it was mentioned that in 1997 two epidemics arose in Algeria and Independent States Community [1]. And as it is not so far from Europe we must attach great importance to this in order to prevent the spread of infection in time. In particular, we should pay attention to the fact that imported cases were diagnosed in neighboring European countries, which is evidence of the ability of the infection to spread quickly. Also, it is important that since 1997 there has been significant progress in modern technologies, as well as in the field of tourism, which leads us to think about a faster spread of the infection.
Keywords: Diphteria; Corynebacterium diphtheria; Epidemiology; Infectious disease outbreaks; Cases among migrants.
Introduction
Diphtheria is an infection caused by Corynebacte-rium species, especially Corynebacterium diphtheria. It causes skin lesions and mucosal infection and can rarely cause focal infection. The course of the infectious process of C. diphtheria infection is influenced by the anatomic site of lesions, the immune status of the human organism, and the production and systemic distribution of toxins [2].
Diphtheria is a toxin-mediated infection and it is an important and potentially fatal threat to patients. Nowadays during the current dramatic influx of refugees into Europe, our objective is to control and prevent the prevalence of infection.
Results
In fact, in 2017, nearly 8,819 cases of diphtheria were reported worldwide, the most since 2004 [9].
One of the studies describes observations on the spread of an infection brought into the country. In this case, we are talking about an outbreak of imported diphtheria with Corynebacterium diphtheriae among migrants arriving in Germany [3].
In 2018, WHO recorded 16,611 new recorded cases of diphtheria. Outbreaks of respiratory diphtheria have been reported in several countries, including Nigeria in 2011 and India during 2010-2016. Refugee resettlement centers (such as Bangladesh) are highly vulnerable, with an increase in diphtheria cases and asymptomatic carriers due to the low availability of public health services. Between 2015 and 2018,
diphtheria outbreaks occurred in Haiti, Venezuela, and Yemen due to socioeconomic crisis or war, resulting in poor access to health care and vaccination [4].
It has been a significant increase in cases of imported, mainly cutaneous, diphtheria caused by toxigenic Corynebacterium diphtheriae among migrants who have recently arrived in Germany since the end of July 2022. Other European countries also have reported similar cases. The list of countries includes Austria, Belgium, France, Norway, Switzerland, and the United Kingdom. One of the researches describes the first epidemiological data officially registered in Germany between 1 January and 30 September 2022. It was noted a total of 44 such cases [3].
Causes of spread
Toxigenic C. diphtheriae-associated wound infections are currently observed more frequently in Europe. This is because refugees travel in poor hygienic conditions. It is often possible to observe that only a few patients received the vaccination. [4].
Talking about the general epidemiology of diphtheria, many studies show us the following analysis, according to which the average incubation period is 1.4 days. On average, untreated cases are colonized within 18.5 days, and 95% are cleared of Corynebacterium diphtheriae within 48 days. Asymptomatic carriers cause 76% fewer cases of infection than symptomatic cases. Receiving 3 doses of diphtheria toxoid vaccine is 87% effective against symptomatic disease and reduces transmission by 60%.
