Theme Shigellae infections. Salmonellae infections. Escherichia infections. Yersiniosis. Rotaviral infection Theme Viral hepatitis A, B, С, d et al. Gastrointestinal infections: guidance, data and analysis
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- Bu səhifədəki naviqasiya:
- Key worlds and phrases
- Acute hepatitis
- Etiology
- GBV-C, or
- Hepatitis C
- Diagnostic criteria of incubation period
- Diagnostic criteria of prodromal (prejaundice, preicteric) period
- Laboratory tests in prodromal period
- Specific tests (markers)
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Differential diagnosis with: Acute intestinal infections, Viral hepatitis, Scarlet fever, Measles, Enteroviral infections, Sepsis, Pseudotuberculosis, Typhoid fever. Yersiniosis Differential diagnosis with Pseudotuberculosis Sign Yersiniosis Pseudotuberculosis Beginning Often subacute Acute
Moderate, increase Severe from the beginning
Not often (41 %) Very often (84 %)
48 %
Conjunctivitis, scleritis 12,6 %
30,1 % Arthralgia 20,9 %
40,1 % Abdominal pain Often
Not often Enteritis, enterocolitis A leading symptom Secondary symptom
Often
Rare Bacteriology Yersinia enterocolitica Yersinia Pseudotuberculosis
Prophylaxis: The following steps can be taken to prevent the spread of Y enterocolitica infection: 1.
Isolation and treatment of ill person, disinfection. 2.
Examination of contact from the epidemic focus for 3 wks (measuring the temperature, skin, throat and feces inspection), 1 bacteriological testing of feces. 3.
Instruct patients and at-risk individuals about appropriate hygiene methods and signs and symptoms of infection 4. Encourage public awareness of Y enterocolitica outbreaks and modes of transmission 5.
Hand washing and control of environmental cross-contamination are principal measures in reducing the spread of enteric pathogens in daycare centers, healthcare settings, and pet-care facilities, as well as within households 6. In blood banks, donors should be asked about any recent symptoms of gastroenteritis 7.
Unwashed raw vegetables, uncooked meats (especially pork), and unpasteurized milk should be avoided
Reservoirs should be eliminated 9.
The contamination of food products should be minimized 10.
Enteric precautions should be instituted in the care of patients who have been hospitalized with infection
syndrome, abdominal syndrome, dyspepsia, hepatosplenomegaly, lymphadenopathy, arthritis, hepatitis, myocarditis, glomerulonephritis, bronchitis and pneumonia, strawberry tongue, ”gloves”, ”socks”, ”hood”- symptoms. VIRAL HEPATITIS
hepatic transaminase level, lasting less than 6 mo. and accompanied with pain, dyspeptic, intoxication and cholestatic syndromes. Chronic hepatitis is defined as a chronic inflammatory reaction in the liver as shown by liver function tests and histology and continuing without improvement for at least six months.
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positive-sense, linear RNA enterovirus of the Picornaviridae family. HAV is an icosahedral nonenveloped virus, measuring approximately 28 nm in diameter. Its resilience is demonstrated by its resistance to denaturation by ether, acid (pH 3.0), drying, and temperatures as high as 56°C and as low as -20°C. The Hepatitis A virus can remain viable for many years. Boiling water is an effective means of destroying it. Chlorine and iodine are similarly effective. Various genotypes of HAV exist; however, there appears to be only 1 serotype. Virion proteins 1 and 3 are the primary sites of antibody recognition and subsequent neutralization. •
virion consisting of a 42-nm spherical, double-shelled particle composed of small spheres and rods and with an average width of 22 nm.
HBV can survive when stored for 15 years at –20°C, for 24 months at –80°C, for 6 months at room temperature, and for 7 days at 44°C. The viral genome of Hepatitis B consists of a partially double-stranded, circular DNA molecule of 3.2 kilobase (kb) pairs that encodes the following 4 overlapping open reading frames: – Gene S codes for Hepatitis B surface antigen (HBsAg), a viral surface polypeptide – Gene C codes for Hepatitis B core antigen (HBcAg), the nucleocapsid protein; it also codes for Hepatitis B e antigen (HBeAg), whose function is unknown – Gene P codes for a DNA polymerase that has reverse transcriptase activity – Gene X codes for the X protein that has transcription-regulating activity
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in diameter, belonging to the family Flaviviridae, genus Flavivirus; HCV can produce at least 10 trillion new viral particles each day. The natural targets of HCV are hepatocytes and, possibly, B lymphocytes. Viral clearance is associated with the development and persistence of strong virus-specific responses by cytotoxic T lymphocytes and helper T cells. In most infected people, viremia persists and is accompanied by variable degrees of hepatic inflammation and fibrosis. •
unique infection that requires Hepatitis B surface antigen (HBsAg) for propagation. Hepatic cell death may occur due to the direct cytotoxic effect of HDV or via a host- mediated immune response. There are three known genotypes of HDV. Genotype I has a worldwide distribution; genotype 2 exists in Taiwan, Japan, and northern Asia; and genotype 3 is found in South America. •
nonenveloped. It has a diameter of approximately 34 nanometers, and it contains a single strand of RNA approximately 7.5 kilobases in length. Five HEV genotypes have been identified
• GBV-C, or Hepatitis G virus (HGV) belongs to the Flaviviridae family. Seven HGV genomes have been described. The isolates from West Africa are referred to as genotype 1 where in 2 subtypes: 1a and 1b are identified. Genotypes 2a and 2b are more frequently detected in North America and Europe; genotypes 3, 4 and 5 are more common in Asia, South-Eastern Asia, and South Africa, respectively. Genotype 6 can be encountered in Southeast Asia. Finally genotype 7 has been reported in China. The genome of the virus is represented by single-chain RNA with positive polarity. The GBV-C genome is similar to Hepatitis C virus (HCV) RNA in its organization. GBV-C RNA codes for two structural proteins (E1 and E2) which are envelope proteins. Five non-structural proteins: NS2, NS3, NS4b, NS5a, and NS5b have been found. These proteins perform the function of protease, helicase, and RNA-dependent RNA- polymerase. Epidemiology: Source of infection – carriers of viruses, ill persons; Way of transmitting: – alimentary for HAV and HEV; – Parenteral, also in case of microtraumas for HBV, HCV, HDV, HGV and HAV (rare); – vertical (perinatal) for HBV, HCV, HDV; – sexual, for HBV, HDV, HCV, HAV (is possible); Susceptibility is high.
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and by direct contact; HEV infection is spread by fecally contaminated water within endemic areas. However, in nonendemic areas, the major mode of the spread of HEV is foodborne, especially consumption of undercooked pork, raw liver, and sausages. Person- to-person contact is the most common means of transmission in Hepatitis A and is generally limited to close contacts. Transmission during the anicteric prodrome is the highest. •
- HAV 70-80 % (children elder than 1 year), Hepatitis A: In developing nations, the age of acquisition is before age 2 years. In Western societies, acquisition is most frequent in persons aged 5-17 years. Within this age range, the illness is more often mild or subclinical; however, severe disease, including fulminant hepatic failure, does occur. - HEV is probably high. Hepatitis E has worldwide distribution, but predominating factors include tropical climates, inadequate sanitation, and poor personal hygiene. It is found most often in developing countries near the equator, in both the Eastern and Western hemispheres. • Outcome Long-term immunity accompanies HAV and HEV infection. Recurrence and chronic Hepatitis do not usually occur. In HEV the overall case fatality rate is 4%, but it is 20% among pregnant women.
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semen, and vaginal secretions); •
- parenteral (with accidental needle sticks or sharing of needles, blood transfusions, and organ transplantation, by means of a contaminated medical equipment, via tattooing, sharing razors, and acupuncture); - vertical (Maternal-fetal transmission during the delivery); - sexual (particularly those who practice unprotected anal intercourse and have infection with human immunodeficiency virus); - contact (household contacts); • Receptivity is the greatest at children of early age and people elder than 30 years. Pathogenesis: Hepatitis A, E 1. Inoculation of the pathogen (small intestine is an atrium for infection). 2. Viremia. 3. Viral fixation on hepatocytes, intracellular localization. 4. Primary replication of the virus. 5. Excretion with bile to intestine. 6. Part of the viruses cause viremia (prodromal period of the disease). 7. Activation of immune system, that causes cytolysis, mesenchimal inflammation and cholestasis. 8.
Immune response, elimination of the virus, recovery.
Hepatocyte Hepatitis B The 5 stages that have been identified in the viral life cycle of Hepatitis B infection. Stage 1: Immune tolerance: lasts approximately 2-4 weeks, represents the incubation period. Active viral replication continues despite little or no elevation in the aminotransferase levels and no symptoms of illness.
effect occurs. HBeAg can be identified, and a decline in the levels of HBV DNA is seen in some patients who are clearing the infection. The duration of this stage is approximately 3-4 weeks (symptomatic period). For patients with chronic infection, 10 years or more may elapse before cirrhosis develops, immune clearance takes place, HCC develops, or the chronic HBeAg-negative variant emerges. Stage 3: Inactive chronic infection: the host can target the infected hepatocytes and HBV. Viral replication is low or no longer measurable, and anti-HBe can be detected. Aminotransferase levels are within the reference range. HBsAg still is present in the serum.
Stage 4: Chronic disease: the emergence of chronic HBeAg-negative disease can occur from the inactive chronic infection stage (stage 3) or directly from the immune active/clearance stage (stage 2).
and antibodies to various viral antigens have been produced. Fulminant hepatic failure is believed to be caused by massive immune-mediated lysis of infected hepatocytes. 1. Inoculation of the pathogen. 2. Viremia. 3. Viral integration and replication in hepatocytes, also in blood cells, bone marrow, lymph nodes, spleen. 4.
Activation of immune system, that causes cytolysis, mesenchimal inflammation and cholestasis. 5. Immune response, elimination or persistence of the virus. Hepatitis C The natural targets of HCV are hepatocytes and, possibly, B lymphocytes. Viral clearance is associated with the development and persistence of strong virus-specific responses by cytotoxic T lymphocytes and helper T cells. In most infected people, viremia persists and is accompanied by variable degrees of hepatic inflammation and fibrosis. The proteolytic cleavage of the virus results in two structural envelope glycoproteins (E1 and E2) and a core protein. Other viral components are nonstructural proteins (NS2, NS3, NS4A, NS4B, NS5A, NS5B, and p7), whose proteins function as helicase-, protease-, and RNA-dependent RNA polymerase, although the exact function of p7 is unknown. These nonstructural proteins are necessary for viral propagation and have been the targets for newer antiviral therapies, such as the direct-acting antiviral agents (DAAs). 1.
Inoculation of the pathogen. 2.
Viremia. 3.
Viral integration and replication in hepatocytes, also to blood cells, bone marrow, lymph nodes, spleen. 4. Activation of immune system with low immune response. 5. Mutation changeability of the virus. 6. Persistence of the virus. Hepatitis D Needs Hepatitis B virus for its replication, develops only in infected HBV patients. Hepatitis G GBV-C predominantly replicates in peripheral blood mononuclear cells, mainly in B and T (CD4+ and CD8+) lymphocytes and bone marrow. HGV replication in peripheral blood monocytes and lymphocytes, and the spleen and bone marrow, combined with long viral persistence suggest that GBV-C replicates predominantly in the hematopoietic system. The hepatotropicity of GBV-C is low. 1. Inoculation of the pathogen. 2. Viremia. 3. Viral integration and replication in hepatocytes, also in blood cells, bone marrow, lymph nodes, spleen. 4.
Activation of immune system, that causes cytolysis, mesenchimal inflammation and cholestasis. 5. Immune response, elimination or persistence of the virus. Classification Type: • typical (icteric); • atypical: - without jaundice (unicteric hepatitis); - effaced; - subclinical hepatitis; - cholestatic hepatitis; - fulminant hepatitis. Severity: • mild • moderate • severe
Course: • acute (2-3 months); • prolonged (3-6 months); • chronic (more than 6 mo.) Periods: • incubation • pre-icteric (prejaundice) • icteric (jaundice) • post-icteric (postjaundice) • recovery Diagnostic criteria of incubation period • Hepatitis A incubation period usually lasts 2-6 weeks. • Hepatitis E incubation period ranges from 2-8 weeks. • Hepatitis B incubation period is 1-6 months. • Hepatitis C incubation period is 8 weeks approximately. • Hepatitis D incubation period for Co-infection is 90 days (range 45-160 days), for superinfection is approximately 2-8 weeks. • Acute Viral Hepatitis G incubation period average is 14-20 days. Diagnostic criteria - absence of clinical signs - viral antigens are present in blood - alanine aminotranspherase (ALT), aspartate aminotranspherase (AST) may be elevated in the end of this period. Diagnostic criteria of prodromal (prejaundice, preicteric) period • mild symptoms of anorexia, fatigue, malaise, myalgia, and mild headache, low-grade fever • rashes (often in HBV-hepatitis) • arthralgias Carole’s triad in Hepatitis B • “flu like syndrome” • Dyspepsia: nausea and vomiting • Disordered gustatory acuity and smell sensations • Weight loss (typically 2-4 kg), dehydration in Hepatitis E • hepatomegaly, pain in right hypochondrium, epigastrium that increases with physical activity • enlargement of ALT and AST, urobilinuria, special hepatitis markers. Laboratory tests in prodromal period • Enlargement of ALT and AST, urobilinuria. • Anti-HAV Ig M, HAV RNA for very short period (Hepatitis A). • HBsAg, HBeAg, HBV DNA and anti-НВс IgM (Hepatitis B). • HBsAg, HBeAg, HBV DNA, anti-НВс IgM and HDVAg, HDV-RNA (Hepatitis Delta coinfection). • HCV RNA (Hepatitis C). • Anti-HEV Ig M, HEV RNA (Hepatitis E). • HGV RNA (Hepatitis G). Diagnostic criteria of jaundice (icteric) period • appearing of dark (tea-colored) urine (urobilinuria, bilirubinuria), clay-colored stools; • jaundice of mucous membranes, sclera, and skin (Pic.) it is less likely in children and is uncommon in infants (no longer than 3 wks in Hepatitis A, E; 1-3 mo in Hepatitis B); • itching; • skin rashes (more often occurs on the lower limbs and may have a vasculitic appearance), a few spider angiomas may appear, palmar or facial erythema in severe cases (Pic.), more likely in Hepatitis B; • hemorrhagic syndrome (petechia with bruising, and bleeding); • hepatomegaly (Pic.), liver is thick and tender; • splenomegaly and cervical adenopathy in Hepatitis B (10-20%); • Approximately 25% of patients with acute HCV infection have jaundice (Pic.), whereas less than one third have hepatomegaly.
• enlargement of ALT and AST, • hyperbilirubinemia with conjugate bilirubin prevalence, • bile pigments in urine are positive, • in cholestasis alkaline phosphatase, cholesterol, GGTP are increased • CBC: mild lymphocytosis • Coagulogram: in Hepatitis A the prothrombin time (PT) usually remains within or near the reference range. In Hepatitis B prothrombine index, fibrinogen are decreased. • serum albumin level decrease Specific tests (markers) • Anti-HAV Ig M is positive at the time of onset of the symptoms up to 3-6 mo, HAV-RNA is positive for few days only in the blood, so in has not diagnostic value (Hepatitis A). • HBsAg, HBeAg, HBV-DNA and anti-НВс IgM (Hepatitis B, acute). HBsAg and total anti-HBc, with a negative test for IgM anti-HBc; the persistence of HBsAg for 6 months (Hepatitis B, chronic) • HBsAg (but may be suppressed to undetectable levels with active HDV replication), HBeAg, HBV-DNA, anti-НВс IgM and HDVAg, anti-HDV IgM, HDV- RNA (Hepatitis Delta coinfection). • HCV-RNA with PCR, anti-HCVcore IgM and IgG with enzyme immunoassay, recombinant immunoassay (acute Hepatitis C). • Anti-HEV Ig M remains detectable for 2 months after the onset of illness, HEV-RNA can be detected just before the onset of clinical symptoms in both blood and stool samples. HEV RNA does not persist for long, becoming undetectable in blood about 3 weeks after the onset of symptoms (Hepatitis E). • HGV RNA by the polymerase chain reaction (PCR) (Hepatitis G). Yüklə 3,37 Mb. Dostları ilə paylaş:
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