Clinical Microbiology Chapter 5 Quiz

Clinical Microbiology 0511 MBO 212

• Course offered by Ahnaf Tahmid Saqif

Brief Introduction to Microbiology of Major Infectious Diseases (Chapter 5)

• This chapter likely covers a broad overview of various infectious diseases from a microbiological perspective.

Microbial Diseases of the Digestive System (Lecture 9)

• This lecture focuses on diseases affecting the digestive system caused by microbes.

Introduction

• Microbial diseases of the digestive system stem from ingesting contaminated food or water containing pathogenic microorganisms or their toxins.
• Pathogens often contaminate food or water after being shed in feces from infected people or animals.
• These diseases typically spread via a fecal-oral cycle.
• Effective food production and handling sanitation procedures break this cycle.

Structure of the Digestive System

• The digestive system is a tube-like structure encompassing the mouth, pharynx (throat), esophagus, stomach, small and large intestines.
• Accessory structures include teeth, tongue, salivary glands, liver, gallbladder, and pancreas.

Dental Caries

• Teeth allow microbial masses (dental plaque) to accumulate, a biofilm type.
• Streptococcus mutans is the primary cariogenic bacterium.
• They metabolize carbohydrates, tolerate acidity, and produce dextran – a gummy polysaccharide.

Dental Caries Pathogenesis

• Caries initiation relies on mutans attachment to the tooth.
• A pellicle (thin film of proteins) coats the tooth surface within minutes.
• Cariogenic bacteria colonize the pellicle and produce dextran within hours.
• Dextran production involves sucrose hydrolysis into fructose and glucose, with glucosyltransferase assembling glucose molecules into dextran, and fructose fermenting into lactic acid.
• Dental plaque consists of bacteria and dextran.
• Lactic acid erodes tooth enamel.
• Untreated enamel erosion allows bacteria to penetrate further into the tooth.
• The bacterial composition changes as decay spreads from enamel to dentin.
• Mutans are present in minimal amounts compared to other bacteria.
• Progression of decay reaches the pulp (containing blood supply and nerve cells).
• Without treatment, infection spreads to soft tissues potentially resulting in abscesses.

Sucrose and Dental Caries

• Dental caries were relatively rare in the Western world until the 17th century.
• Sucrose introduction correlates with a rise in caries.
• High-starch diets show lower caries rates unless sucrose is included.

Prevention

• Sugar alcohols (e.g., mannitol, sorbitol, xylitol) are not cariogenic, thus used in sugar-free foods.
• Effective prevention involves minimizing sucrose intake, regular brushing and flossing, professional cleanings, and fluoride application.

Hepatitis

• Hepatitis is liver inflammation.

• Multiple viruses cause hepatitis with more potentially undiscovered or unidentified.

• Infections by other viruses (e.g., Epstein-Barr Virus (EBV), cytomegalovirus (CMV)) might also cause hepatitis sporadically.

• Detailed table on various types of hepatitis (pathogen, symptoms, incubation periods, transmission, diagnostic tests, treatments, and vaccines)

HBV (Hepatitis B Virus)

• HBV is a large, partially double-stranded DNA virus with an envelope.
• Patient serum contains three different HBV particles: complete virion (Dane particle), smaller spherical particles, and filamentous particles.

HBV Infection

• HBV infection is associated with chronic liver diseases (CLD) ranging from hepatitis to fibrosis, cirrhosis, and finally hepatocellular carcinoma (HCC) over decades.
• CLD pathogenesis is marked by the persistence of immune responses against virus-infected hepatocytes.
• HCC is a significant cause of cancer-related mortality.

Acute HBV Infection

• Many HBV infections are subclinical, meaning people don't exhibit symptoms, but in others, symptoms include fever, nausea, abdominal pain, jaundice, and dark urine.
• In a small number of cases, fulminant hepatitis (massive liver damage) may occur.

Chronic HBV Infection

• Hepatitis lasting more than six months is classified as chronic.
• High chronic carrier rates seen in people infected during childhood.
• Likelihood of chronic infection diminishes as age increases.

Risk Population

• Health care workers and IV drug users have higher exposure and infection risks due to their frequent exposure to blood.
• Children born to HBV-positive mothers also face elevated risk.

Transmission

• High-prevalence regions (Asia): HBV acquisition is often perinatal. The immune system demonstrates tolerance for the virus resulting in chronic infection.
• Low-prevalence regions (West): Transmission usually comes from exposure to infected blood or bodily fluids. Commonly associated with risky behaviours in young adults like intravenous drug use and promiscuous sex. In these scenarios, it often resolves without progression to chronic disease.

HBV Pathogenesis

• HBV's partially double-stranded DNA becomes fully double stranded upon infection.
• The viral genome acts as a template for sub-genomic RNA and pre-genomic RNA transcription within infected cells.
• Viral proteins trigger innate immune responses, damage mitochondria, and stress endoplasmic reticulum, leading to inflammation and liver damage.
• A weak immune response allows the virus to persist for years.

Diagnosis

• Diagnosis relies on symptoms and liver functionality tests.
• Serologic tests detect HBV antigens (HBsAg).
• Presence of HBsAg confirms active infection.

Prevention

• Precautions, such as disposable needles, barrier-type contraception, and blood screening reduce risk.
• HBV vaccines are widespread in childhood immunization schedules.

Test your knowledge on the microbiology of major infectious diseases, particularly focusing on microbial diseases of the digestive system. This quiz covers various pathogens, their transmission, and effective sanitation practices. Dive into the complexities of how these diseases affect the digestive system and their impact on public health.