Case Study Rubric: Microbiology For The Assignment

Case Study Rubric Microbiologyfor The Case Study Assignment The Curren

Create a detailed case study for a microbial infection selected from the current pathogen list, including patient presentation, pathogen description, epidemiology, pathogenesis, and treatment options. Incorporate at least 3-4 key referenced points in each of the five areas outlined by the case study chart. Include two discussion questions with complete answers that connect to course material. Use credible sources such as scientific literature, CDC, WHO, textbooks, and online databases. Cite all sources in APA format and include a references section. Submit your case study via Blackboard in Unit 5, naming the file as specified. Ensure your submission is comprehensive, well-organized, and approximately several pages long, including figures or illustrations as needed.

Sample Paper For Above instruction

Title: Case Study of Mycobacterium tuberculosis - A Tuberculosis Infection

Introduction and Patient Presentation

A 45-year-old male patient presents with a persistent cough lasting over three weeks, hemoptysis, night sweats, weight loss, and fever. The patient reports recent travel to regions with high tuberculosis prevalence and a history of close contact with individuals diagnosed with respiratory infections. Physical examination reveals bilateral crackles in the lungs. Laboratory findings include a positive sputum acid-fast bacilli (AFB) smear and chest radiographs showing cavitary lesions in the upper lobes. The clinical presentation, history, and lab findings suggest a case of pulmonary tuberculosis caused by Mycobacterium tuberculosis.

Description of the Infectious Agent

Mycobacterium tuberculosis is a slow-growing, obligate aerobe bacterium classified within the genus Mycobacterium, Family: Mycobacteriaceae. It is a Gram-positive, acid-fast bacillus with a characteristic lipid-rich cell wall that confers resistance to many common antibiotics and environmental stresses. The organism has a unique capacity to form granulomas in host tissue, allowing it to persist for long periods. It targets macrophages, displaying strong tropism for lung tissue, which is its primary site of infection. M. tuberculosis can form dormant states, contributing to latent infections. It can be distinguished from other mycobacteria through molecular techniques such as PCR and specific biochemical tests like niacin accumulation and the presence of the catalase enzyme.

Epidemiology

Global tuberculosis incidence remains high, with approximately 10 million new cases reported annually worldwide (World Health Organization, 2021). The primary portal of entry is the respiratory tract, with inhaled aerosolized droplets containing the bacteria. The source is often an individual with active pulmonary disease; transmission occurs via airborne droplets. M. tuberculosis has a significant association with socio-economic factors, including poverty and overcrowding. Regions in Southeast Asia, Africa, and parts of Eastern Europe show higher prevalence. The pathogen has a zoonotic potential in rare cases involving infected animals, but human-to-human transmission predominates. Outbreaks are seasonal and often occur in crowded settings, such as prisons and shelters. Ecological niches include urban environments with dense populations, and reservoirs include infected humans with active disease.

Pathogenesis

M. tuberculosis causes a spectrum of pulmonary and extrapulmonary diseases. The primary infection results when the bacteria are inhaled into the alveoli, where macrophages attempt to ingest and destroy them. However, M. tuberculosis possesses mechanisms to survive within macrophages, evading the immune response. The infection leads to the formation of granulomas—organized collections of immune cells attempting to contain the bacteria. The disease manifests with symptoms such as cough, hemoptysis, weight loss, and night sweats, typically following a latent period. In some cases, the bacteria disseminate via lymphatic or hematogenous routes, causing miliary tuberculosis affecting multiple organs. Long-term sequelae can include pulmonary fibrosis and bronchiectasis, with the possibility of reactivation years later, especially in immunocompromised individuals. Disease progression depends on host immunity and bacterial virulence factors (Philips & Ernst, 2012).

Prophylaxis and Treatment

Standard treatment involves a multi-drug regimen, including isoniazid, rifampin, ethambutol, and pyrazinamide for the initial two months, followed by a continuation phase with isoniazid and rifampin for an additional four months. Directly Observed Therapy (DOT) is recommended to ensure adherence and prevent resistance. BCG vaccine, derived from Mycobacterium bovis, offers partial protective immunity, primarily against severe childhood TB but is less effective for pulmonary TB in adults. Anti-tubercular drugs have significantly reduced disease burden, although drug-resistant strains such as MDR-TB and XDR-TB are emerging challenges (WHO, 2021). Treatment is usually curative if completed properly, but long-term surveillance is crucial to prevent relapse and resistance. Latent tuberculosis infection (LTBI) can be managed with prophylactic isoniazid therapy. During treatment, monitoring for hepatotoxicity and drug interactions is essential (Lawn & Zumla, 2011).

Discussion Questions

Question 1: How does Mycobacterium tuberculosis evade the host immune response, leading to latent infection?

Answer: M. tuberculosis evades immune destruction by inhibiting phagosomal maturation within macrophages, preventing fusion with lysosomes. It also modulates host cytokine responses, promoting granuloma formation that contains the bacteria but allows persistence in a dormant state. The lipid-rich cell wall protects against oxidative stress, and the bacterium can enter a non-replicating, dormant phase resistant to antibiotics and immune clearance (Flynn & Chan, 2001).

Question 2: What strategies are being developed to combat drug-resistant strains of M. tuberculosis?

Answer: New strategies include developing novel antibiotics targeting unique bacterial enzymes, host-directed therapies that modulate immune responses, and vaccines with improved efficacy. Researchers are also exploring ways to shorten treatment duration and prevent the emergence of resistance through molecular diagnostics that enable rapid detection of resistant strains, ensuring appropriate therapy (Dheda et al., 2017).

References

• Flynn, J. L., & Chan, J. (2001). Immunology of tuberculosis. Annual Review of Immunology, 19, 93-129.
• Lawn, S. D., & Zumla, A. I. (2011). Tuberculosis. Lancet, 378(9785), 57-72.
• Philips, J. A., & Ernst, J. D. (2012). Tuberculosis pathogenesis and immunity. Annual Review of Pathology, 7, 351-376.
• World Health Organization. (2021). Global Tuberculosis Report 2021. WHO.
• Dheda, K., et al. (2017). The Lancet Respiratory Medicine, 5(10), 911-927.