Clinical Microbiology Lecture Notes PDF

Summary

These notes cover clinical microbiology, focusing on infectious diseases, particularly microbial diseases of the digestive system, including dental caries. It details the structure of the digestive system, pathogenesis of dental caries, and different types of hepatitis (with a focus on HBV).

Full Transcript

Clinical Microbiology 0511 MBO 212 Ahnaf Tahmid Saqif Lecturer Brief Introduction to Microbiology of Major Infectious Diseases Chapter-5 Microbial Diseases of the Digestive System Lecture-9 Introduction Microbial diseases of the digest...

Clinical Microbiology 0511 MBO 212 Ahnaf Tahmid Saqif Lecturer Brief Introduction to Microbiology of Major Infectious Diseases Chapter-5 Microbial Diseases of the Digestive System Lecture-9 Introduction Microbial diseases of the digestive system result from ingesting food or water contaminated with pathogenic microorganisms or their toxins. These pathogens usually enter the food or water supply after being shed in the feces of people or animals infected with them. Therefore, microbial diseases of the digestive system are typically transmitted by a fecal–oral cycle. This cycle is interrupted by effective sanitation practices in food production and handling. Structure of the Digestive System The digestive system is essentially a tubelike structure containing the mouth, pharynx (throat), esophagus, stomach, and the small and large intestines. It also includes accessory structures such as the teeth and tongue. Certain other accessory structures such as the salivary glands, liver, gallbladder, and pancreas Dental Caries The teeth are hard which allows masses of microorganisms and their products to accumulate. These accumulations, called dental plaque, are a type of biofilm. The most important cariogenic (caries-causing) bacterium is Streptococcus mutans, a gram-positive coccus that is capable of metabolizing a wide range of carbohydrates, tolerates a high level of acidity, and synthesizes dextran*. * Dextran a gummy polysaccharide of glucose molecules which is an important factor in the formation of dental plaque. Dental Caries Pathogenesis The initiation of caries depends on the attachment of S. mutans to the tooth. These bacteria do not adhere to a clean tooth, but within minutes a freshly brushed tooth will become coated with a pellicle (thin film) of proteins from saliva. Within a couple of hours, cariogenic bacteria become established on this pellicle and begin to produce a dextran. Dental Caries Pathogenesis In the production of dextran, the bacteria first hydrolyze sucrose into its component monosaccharides, fructose and glucose. The enzyme glucosyltransferase then assembles the glucose molecules into dextran. The residual fructose is then fermented into lactic acid. Accumulations of bacteria and dextran adhering to the teeth make up dental plaque. Dental Caries Pathogenesis Lactic acid produced by the plaque can break down enamel of the teeth. If the initial penetration of the enamel by caries remains untreated, bacteria can penetrate into the interior of the tooth. The composition of the bacterial population involved in spreading the decayed area from the enamel into the dentin is entirely different from that of the population initiating the decay. The dominant microorganisms are gram-positive rods and filamentous bacteria; S. mutans is present in small numbers only. Dental Caries Pathogenesis The decayed area eventually advances to the pulp, which connects with the tissues of the jaw and contains the blood supply and the nerve cells. Once this stage is reached, root canal therapy is required to remove the infected and dead tissue and to provide access for antimicrobial drugs that suppress renewed infection. If untreated, the infection may advance from the tooth to the soft tissues, producing dental abscesses caused by mixed bacterial populations that contain many anaerobes. Sucrose and Dental Caries Although dental caries is probably one of the more common infectious diseases in humans today, it was scarce in the Western world until about the seventeenth century. The introduction of table sugar, or sucrose, into the diet is highly correlated with our present level of caries in the Western world. People living on high-starch diets have a low incidence of tooth decay unless sucrose is also a significant part of their diet. Prevention Sugar alcohols, such as mannitol, sorbitol, and xylitol, are not cariogenic. This is why these sugar alcohols are used to sweeten “sugarless” candies and chewing gum. The best strategies for preventing dental caries are a minimal ingestion of sucrose; brushing, flossing, and professional cleaning to remove plaque; and the use of fluoride. Professional removal of plaque and tartar at regular intervals lessens the progression to periodontal disease. Hepatitis Hepatitis is an inflammation of the liver. At least five different viruses cause hepatitis, and probably more remain to be discovered or become better known. Hepatitis is also an occasional result of infections by other viruses such as Epstein-Barr virus (EBV) or cytomegalovirus (CMV). HBV Hepatitis B virus (HBV) is a large virus containing partially double stranded DNA and covered by an envelope. The serum from patients with hepatitis B contains three distinct particles. The largest is the complete virion; it is infectious and capable of replicating. It is often referred to as a Dane particle. There are also smaller spherical particles, about half the size of a complete virion, and filamentous particles, which are tubular particles similar in diameter to the spherical particles but about ten times as long. HBV Infection HBV infection is associated with chronic liver diseases (CLD), which progress from hepatitis to fibrosis, cirrhosis, and finally hepatocellular carcinoma (HCC) over 30–50 years. The pathogenesis of CLD is characterized by persistent immune responses against virus infected hepatocytes. HCC is the sixth most prevalent cancer worldwide, with about 600,000 newly diagnosed cases annually, and the second leading cause of cancer deaths. Acute HBV Infection Many cases of acute hepatitis B are subclinical; meaning the infected person is often entirely unaware. In about a third of the cases, the patient exhibits symptoms of disease— the person feels unwell and often suffers from low-grade fever, nausea, and abdominal pain. Eventually, jaundice, dark urine, and other evidence of liver damage appears. However, in a few cases (less than 1%), the patient develops fulminant hepatitis, causing sudden, massive liver damage; survival without a liver transplant is uncommon. Chronic HBV Infection If a case of hepatitis persists for more than 6 months, the condition is considered to have become chronic. People infected when very young are the most likely to become chronic carriers. The risk for infants is about 90%; in children of 1 to 5 years, about 25–50%. Adolescents and young adults have a much lower risk, only 6–10%. Overall, up to 10% of infected patients become chronic carriers of the virus. Risk Population Health care workers and others who are in daily contact with blood have a considerably higher incidence of hepatitis B than members of the general population. Intravenous drug users often share syringes and needles and fail to sterilize them properly; as a consequence, they also have a high incidence of hepatitis B. Children born to HBV-positive mothers. Transmission In high-prevalence (Asian) countries, HBV infection tends to be acquired around the time of birth (perinatal) from infected mothers. As a consequence, the immune system does not recognize a difference between the virus and the host, and a high level of immunologic tolerance ensues. Because of this tolerance, the infection is not accompanied by acute hepatitis; instead, a chronic, usually lifelong infection is established. This is the case in about 90% of infected persons. Transmission In low-prevalence (Western) countries, most acute infections by HBV occur from exposure to infected blood or other body fluids. It is often a disease of young adults participating in risky behaviours—injection drug use or sexual promiscuity. Infected people who are immunocompetent develop a strong immune response, and the virus is cleared in all but about 1% of those infected. These patients have a much lower incidence of chronic disease and of liver cancer. HBV Pathogenesis 1. Upon infection, the partially double stranded viral DNA is made fully double stranded. 2. The HBV genome then appears as a supercoiled mini-chromosome in the nuclei of infected cells, and this acts as a template for the transcription of sub-genomic RNAs and a pre-genomic RNA. 3. Both the RNAs migrate to the cytoplasm where the sub-genomic RNA is translated into Hepatitis B X-antigen (HBx), polymerase and other proteins. 4. HBV encoded proteins then stimulate innate immune response, damage the mitochondria and put severe stress on endoplasmic reticulum. 5. All of these effects result in the inflammation of liver. If the immune response is weak, the virus is hard to clear and it keeps damaging the liver for a number of years. Diagnosis The diagnosis of HBV is usually based on symptoms, followed by tests of liver function. Serologic tests can detect HBV antigens and antibodies. The presence of hepatitis B surface antigen (HBsAg) indicates the presence of the virus in the blood. After the virus is cleared, antibody appears, and the patient is considered immune. Prevention Precautions such as disposable needles and syringes and the use of barrier-type contraception is important. Screening of transfused blood has also greatly reduced the risk. The introduction of HBV vaccines has become widespread worldwide and is now part of the childhood immunization schedule in many countries.

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