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The human body hosts roughly 10¹⁴ microorganisms—about 10 times the number of human cells—forming a complex ecological community essential for health. (NCBI Source)
Centers for Disease Control and Prevention. “Chemical Disinfectants.”
Guideline for Disinfection and Sterilization in Healthcare Facilities, 2008.
cdc.gov/chemical-disinfectants
Antimicrobial Resistance: The Global Crisis We're Still Underestimating
Antimicrobial Resistance: The Global Crisis We're Still Underestimating
By MBLOGSTU 04 July 2025
If the COVID-19 pandemic taught the world one thing, it’s that microbial threats respect no borders. Yet even as the world raced to contain a novel virus, another slower, more insidious pandemic has been taking root—antimicrobial resistance (AMR). It’s not dramatic like COVID, but it’s deadlier, more complex, and frighteningly under-prioritized.
Recent projections from Wellcome Trust suggest that 39 million people may die from drug-resistant bacterial infections by 2050—that’s nearly three people every minute for the next 25 years. But it’s not just the numbers that should concern us; it's the multifaceted nature of this threat and our fragmented response.
AMR Isn’t Just a Medical Problem—It’s a Systems Failure
Historically, we’ve viewed AMR as a clinical challenge: doctors overprescribing antibiotics, patients not completing courses. But this reductionist lens obscures a much broader truth. AMR is a systems-level failure—of health policy, of agriculture, of environmental stewardship, and increasingly, of innovation.
A case in point: microplastics. A groundbreaking 2025 study reveals that nanoplastics can promote biofilm formation in E. coli, effectively turbocharging resistance and pathogenicity. These microplastic “training camps” for bacteria are now ubiquitous in water sources, soils, and even our food.
The One Health Imperative
We’ve ignored for too long the connections between human, animal, and environmental health. In fact, up to 80% of all antibiotics globally are used in livestock—not to treat disease, but to promote growth. Waste from these farms, rich in resistant bacteria and drug residues, enters waterways and soils, creating what scientists call environmental resistomes.
WHO’s “One Health” strategy, aiming to link these sectors through integrated surveillance and action, is promising. But despite its adoption in national plans, implementation remains patchy, underfunded, and largely aspirational.
Science Offers Hope—but Needs Investment
The good news? Science is not standing still. In Australia, researchers have found that the hemolymph of oysters contains peptides capable of penetrating biofilms and boosting antibiotics' power by up to 32 times. AI-driven models are now designing antimicrobial peptides and phage cocktails tailored to specific infections. And antimicrobial photodynamic therapy (aPDT)—where light and photosensitizers kill microbes without triggering resistance—is showing strong potential.
The bad news? Drug companies have largely abandoned the antibiotics market. With high development costs and low returns, new antibiotics often fail to break even. If we don’t radically rethink antibiotic R&D incentives, the pipeline will remain dry—just when we need it most.
Data and Diagnostics: A Weak Link in a Digital Age
Digital health is booming, yet AMR surveillance is shockingly outdated. Antibiotic susceptibility testing (AST) remains slow and centralized. Portable, AI-powered AST tools are emerging, but affordability and access are major barriers—especially in low- and middle-income countries, where less than 7% of patients with resistant infections receive appropriate treatment.
AI and machine learning models that could revolutionize resistance tracking and antibiotic discovery are hindered by fragmented data and inconsistent standards.
What Needs to Change—Now
Scale One Health from policy to practice with cross-sector investment and shared accountability.
Ban or strictly limit non-therapeutic antibiotic use in agriculture.
Incentivize antibiotic innovation via market-pull strategies.
Accelerate diagnostics and surveillance in both high- and low-resource settings.
Tackle environmental drivers—like plastic pollution and pharmaceutical waste.
Conclusion: AMR Is the Defining Health Challenge of Our Time
We often imagine future pandemics as sudden viral outbreaks. But the real threat may be slow-burning, gene-driven, and quietly evolving beneath our feet, in our food, and in our hospitals.
If AMR were a virus, we would have declared a global emergency by now. It's time we treat it that way.
Retroviruses are a type of RNA virus that replicate through a DNA intermediate. They integrate their genetic material into the host genome, enabling efficient replication. This lifecycle ensures their persistence and spread in host populations.
Source: Biorender.com [6,7]
Binding
The first step in the retrovirus life cycle is the binding of the virus to the host cell. This binding is mediated by specific viral surface proteins interacting with receptors on the host cell surface.
The list of specific receptors is provided in Table 1.
Table 1. List of Specific Receptors in Retroviruses
Name of Virus
Name of Receptor
References
Ecotropic MLV
CAT-1 (amino-acid transporter)
[1,10]
HIV
CD4 (T-cell surface marker)
[2]
HTLV
GLUT-1 (glucose transporter)
[3]
Amphotropic MLV
PIT-2 (phosphate transporter)
[4,9]
Gibbon Ape Leukemia Virus (GaLV)
PIT-1 (phosphate transporter)
[5]
Fusion
After binding to the host cell, the retrovirus must enter the host cell's cytoplasm to initiate infection. This is achieved through the fusion of the viral envelope with the host cell membrane. Fusion allows the viral core containing the viral RNA and associated enzymes to enter
the host cell.
Reverse Transcription
Once inside the host cell, the retroviral RNA genome is reverse transcribed into double-stranded DNA by the viral enzyme reverse transcriptase. This process involves the synthesis of a complementary DNA (cDNA) strand from the viral RNA template,
followed by the synthesis of a second DNA strand to form a double stranded DNA molecule. Reverse transcription takes place within the cytoplasm of the host cell.
Integration
The newly synthesized viral DNA is transported into the nucleus of the host cell, where it integrates into the host cell's chromosomal DNA. This integration is mediated by the viral enzyme integrase, which cleaves the host cell DNA and inserts the viral DNA into the host genome. Once integrated, the viral DNA is referred to as a provirus.
Transcription
Once integrated into the host genome, the proviral DNA can be transcribed by the host cell's RNA polymerase machinery. This results in the synthesis of viral messenger RNA (mRNA) transcripts, which can then be translated into viral proteins.
Translation
The viral mRNA transcripts produced by the host cell are translated by the host cell's ribosomes into viral proteins. These viral proteins include structural proteins (such as capsid proteins) and enzymes required for viral replication.
Assembly
The newly synthesized viral proteins and viral RNA molecules are assembled into new virus particles, or virions, within the cytoplasm of the host cell. The structural proteins encapsulate the viral RNA to form the viral core, while other viral proteins contribute to the
formation of the viral envelope.
Budding
Once assembled, the new virus particles bud from the host cell membrane, acquiring a lipid envelope derived from the host cell membrane embedded with viral glycoproteins. This budding process allows the newly formed virus particles to acquire their final structure and become infectious.
Release
The mature virus particles are released from the host cell, either by budding off from the cell surface or through cell lysis, where the host cell is destroyed, releasing the viral particles into the extracellular environment. These released virus particles can then infect new host cells, continuing the cycle of infection.
Conclusion
This complete cycle allows retroviruses to efficiently infect host cells, replicate their genetic material, and produce new virus particles, facilitating the spread of infection within a host organism and between individuals.
References
1. Kim JW, Closs EI, Albritton LM, Cunningham JM. Transport of cationic amino acids by the mouse ecotropic retrovirus receptor. Nature. 1991;352:725–728.
2. Maddon PJ, Dalgleish AG, McDougal JS, et al. The T4 gene encodes the AIDS virus receptor. Cell. 1986;47:333–348.
3. Manel N, Kim FJ, Kinet S, et al. The ubiquitous glucose transporter GLUT-1 is a receptor for HTLV. Cell. 2003;115:449–459.
4. Miller DG, Miller AD. A family of retroviruses that utilize related phosphate transporters for cell entry. J Virol. 1994;68:8270–8276.
5. O'Hara B, Johann SV, Klinger HP, et al. Characterization of a human gene conferring sensitivity to infection by gibbon ape leukemia virus. Cell Growth Differ. 1990;1:119–127.
7. Team, B. (2020). Retrovirus Life Cycle. BioRender.
8. Van Zeijl M, Johann SV, Closs E, et al. A human amphotropic retrovirus receptor is a member of the gibbon ape leukemia virus receptor family. Proc Natl Acad Sci U S A. 1994;91:1168–1172.
The immune system is a complex network of cells, tissues, and organs that work together to protect the body from harmful pathogens such as bacteria, viruses, fungi, and parasites. In addition to defending against infections, the immune system also plays a critical role in eliminating damaged or abnormal cells, such as cancerous cells. The immune system has two main types of defenses: innate immunity and adaptive immunity, each with its own specialized functions and characteristics.
Figure 1. Innate Immunity Versus Adaptive Immunity (Source: Biorender.com)
Innate Immunity: The body's first line of defense, offering immediate but nonspecific protection against pathogens.
Adaptive Immunity: A more specific and adaptable defense mechanism that is activated upon exposure to pathogens and improves with subsequent exposures.
Figure 2. Stages of Adaptive Immune Response (Source: Biorender.com)
2. Components of the Immune System
Figure 3. Immune Organs in the Human Body (Source: Biorender.com)
The immune system includes several key components, each playing a vital role in defending the body:
a) Primary Organs:
Figure 4. Stem Cell Differentiation from Bone Marrow (Source: Biorender.com)
Bone Marrow: The site of origin for all immune cells. It produces white blood cells, red blood cells, and platelets.
Thymus: A small organ located in the chest, where T lymphocytes (T cells) mature before being released into the bloodstream.
Figure 5. Anatomy of Thymus (Source: Biorender.com)
b) Secondary Organs:
Figure 6. Lymph Node Structure and Location of Immune Cells (Source: Biorender.com)
Lymph Nodes: Distributed throughout the body, lymph nodes filter lymph fluid and trap pathogens. They are also sites where immune cells interact with antigens.
Spleen: Filters blood, removes old red blood cells, and activates immune responses to blood-borne pathogens.
Mucosal-associated lymphoid tissues (MALT): These include structures like the tonsils, Peyer’s patches in the intestines, and other lymphoid tissues found in mucosal surfaces, playing an important role in immune responses to pathogens entering through mucosal surfaces.
Leukocytes (White Blood Cells): Key players in immune defense, including various subtypes:
Neutrophils: The first responders to infection and the most abundant white blood cells.
Macrophages: Engulf and digest pathogens and dead cells; also play a role in activating adaptive immunity.
Dendritic Cells: Serve as antigen-presenting cells (APCs), displaying antigens to T cells and initiating adaptive immunity.
Natural Killer (NK) Cells: Specialized to kill virus-infected cells and tumor cells.
Lymphocytes: Include B cells and T cells, which play a central role in adaptive immunity.
d) Molecules of the Immune System:
Antibodies (Immunoglobulins): Produced by B cells, antibodies bind to pathogens and neutralize them or mark them for destruction.
Figure 8. Effector Functions of Antibodies (Source: Biorender.com)
Cytokines: Small signaling molecules that regulate immune cell function, inflammation, and hematopoiesis.
Complement Proteins: A group of proteins that enhance the ability of antibodies and phagocytic cells to clear pathogens.
3. Types of Immunity
a) Innate Immunity
Innate immunity is the body’s first line of defense, activated immediately after pathogen detection. It is nonspecific and includes the following:
Physical Barriers.: These are the first defense against pathogens and include the skin, mucous membranes, and secretions like tears and saliva.
Phagocytic Cells: These cells engulf and digest pathogens. Key phagocytes include neutrophils, macrophages, and dendritic cells.
Inflammation: A localized response to infection characterized by redness, swelling, heat, and pain, aimed at recruiting immune cells to the site of infection.
Natural Killer (NK) Cells: Specialized cells that detect and kill infected or abnormal cells, particularly virus-infected cells.
Complement System: A group of proteins that can kill pathogens directly or mark them for destruction by phagocytes.
Key Features of Innate Immunity:
Rapid Response: Innate immunity is activated within minutes to hours after infection.
Nonspecific: It does not target specific pathogens but rather responds to general features shared by many pathogens (e.g., bacterial cell walls).
No Memory: Once an infection is cleared, innate immunity does not retain any specific information about the pathogen for future encounters.
b) Adaptive Immunity
Adaptive immunity is more specific and takes longer to develop but is highly effective and provides long-lasting protection. Key features of adaptive immunity include:
Specificity: Adaptive immunity targets specific pathogens with high precision.
Memory: Adaptive immunity remembers pathogens it has encountered, enabling a faster and more efficient response if the pathogen is encountered again.
The adaptive immune response involves B cells and T cells, which respond to specific pathogens and provide lasting immunity.
B Cells: B cells are responsible for the production of antibodies. When activated by an antigen, B cells differentiate into plasma cells that secrete antibodies. These antibodies bind to pathogens, neutralizing them or marking them for destruction by other immune cells.
T Cells: T cells are involved in recognizing and responding to infected or abnormal cells:
Figure 9.TH1 Cells Help Macrophages Kill Intracellular Bacteria (Source: Biorender.com)
Helper T Cells (CD4+): Assist B cells in producing antibodies and activate cytotoxic T cells and macrophages.
Cytotoxic T Cells (CD8+): Directly kill infected or cancerous cells by recognizing specific antigens presented on the cell surface.
Regulatory T Cells: Regulate immune responses to prevent excessive reactions or autoimmunity.
Key Features of Adaptive Immunity:
Delayed Response: Adaptive immunity takes several days to fully activate.
Antigen Specificity: It specifically targets the antigens of pathogens.
Memory Formation: After the first encounter with a pathogen, memory B and T cells are created. If the pathogen is encountered again, the response is faster and more robust.
4. Antigen Presentation and Immune Activation
Antigen Presentation: The immune system identifies pathogens through molecules called antigens. Antigens are often foreign proteins or polysaccharides present on the surface of pathogens.
MHC Molecules: Antigens are presented on the surface of cells by proteins called major histocompatibility complex (MHC) molecules. There are two types of MHC molecules:
MHC Class I: Present on all nucleated cells and recognized by cytotoxic T cells (CD8+).
MHC Class II: Present on antigen-presenting cells (APCs) like dendritic cells and macrophages and recognized by helper T cells (CD4+).
When an APC presents an antigen via MHC molecules, T cells recognize and bind to it, triggering an immune response.
5. Immune Memory
One of the most important aspects of adaptive immunity is the formation of immune memory. After the immune system successfully combats a pathogen, memory B cells and memory T cells remain in the body for years, or even a lifetime. If the same pathogen enters the body again, these memory cells quickly recognize it and mount a faster, stronger response.
This principle is the basis of vaccination, where an organism is exposed to a harmless form of a pathogen to trigger the production of memory cells without causing illness.
6. Disorders of the Immune System
Immune system dysfunction can lead to a variety of disorders:
Autoimmune Diseases: Conditions where the immune system mistakenly attacks the body’s own tissues [e.g., rheumatoid arthritis, Systemic lupus erythematosus (SLE), type-1 diabetes, psoriasis, coeliac disease, multiple sclerosis].
Immunodeficiencies: Disorders that impair the immune system, making individuals more susceptible to infections. HIV/AIDS is a well-known immunodeficiency. It can be futher divided into primary immunodeficiencies and severe combined immunodeficiencies. The majority of primary immunodeficiency cases are identified in young children, and patients are often more susceptible to infections. However, severe combined immunodeficiencies (SCIDs) are a category of uncommon, monogenic disorders characterised by an early start and a substantial inhibition in T cell development.
Hypersensitivity: Allergic reactions occur when the immune system overreacts to harmless substances such as pollen, food,or drugs. Common allergens includes medication, venoms from insect sting and bites, contact allergies from metal or fragrance, mold, house dust mites, pets and animals from farms, etc.
7. Vaccination and Immunization
Vaccination is a medical intervention that stimulates the immune system to develop protection against pathogens. Vaccines contain weakened or inactivated pathogens or pathogen components that do not cause disease but stimulate an immune response.
Types of vaccines:
Live Attenuated (weakened or inactivated) Vaccines: Contain weakened pathogens that can still replicate but cannot cause disease (e.g., measles, mumps, rubella, influeza, oral polio, typhoid, Japanese encephalities, Bacillus Calmette-Guerin (BCG), varicella zoster, yellow fever, and so on).
Killed whole organism: Contain killed pathogens (e.g., polio vaccine, influenza, Japanese encephalitis, hepatitis A, rabies, Whole-cell pertusis).
Subunit Vaccines (purified protein, recombinant protein, polysachharide, peptide) : Contain pieces of pathogens, such as proteins or sugars (e.g., hepatitis B vaccine, Pertussis, influenza, meningococcal, penumococcal, typhoid).
Toxoid: Toxoids (e.g., diphtheria and tetanus vaccines) are non-toxic bacterial toxins that still have the ability to stimulate antitoxin production.
Virus like particles (VLPs): Virus-like particles (VLPs) are particles that self-assemble as a result of the expression of proteins encoding capsids, cores, or envelopes of viruses, or even preparations of monolayered particles obtained from a multilayered virus. e.g. Human papillomavirus vaccines
Outer membrane vesicle: Spherical buds derived from outer membrane of Gram-negative bacteria filled with periplasmic content. e.g. Group B meningococcal vacccine
Protein-polysachharide conjugate:Polysaccharide vaccines for Haemophilus influenzae type b (Hib) were first used in 1985, but they were quickly replaced by protein-polysaccharide conjugate vaccines in 1989. These vaccines contained the Hib polysaccharide polyribosyl ribitol phosphate chemically conjugated to a protein carrier, such as diphtheria toxoid, tetanus toxoid, or meningococcal outer membrane protein.
Viral vectored vaccines:Viral vector vaccines remain one of the finest techniques for induction of substantial humoral and cellular immunity against human illnesses.Numerous viruses from various families and origins, such as vesicular stomatitis virus, rabies virus, parainfluenza virus, measles virus, Newcastle disease virus, influenza virus, adenovirus, and poxvirus, are regarded as prominent viral vectors. ERVEBO® is a replication-competent, live, attenuated recombinant vesicular stomatitis virus (VSV) used to prevent Ebola virus infection.
Nuclei Acid Vaccine: Nucleic acid vaccines are a type of genetic vaccine that utilize genetic material, specifically DNA or RNA, to instruct cells in the body to produce a protein associated with a pathogen, which then triggers an immune response. These vaccines are distinct from traditional vaccines, which usually contain inactivated or attenuated pathogens, or proteins derived from pathogens.
The two main types of nucleic acid vaccines are: DNA Vaccines: Contain a small, circular piece of DNA that encodes the target antigen. RNA Vaccines: Contain mRNA (messenger RNA) that encodes the target antigen. For instance, the genetic material, RNA in the case of Moderna and Pfizer/BioNTech vaccines, encodes a particular viral protein. The protein is further identified by the immune system triggering a specific response as on the case of SARS-CoV-2 infection.
Bacterial vectored vaccines: These are a type of genetically modified vaccine where harmless bacteria are used as vectors (carriers) to deliver antigens from a pathogen into the body, stimulating an immune response. These vaccines utilize bacteria that have been engineered to carry and express a gene (often from a virus or other pathogen) that encodes an antigen. When the vector bacteria are introduced into the body, they deliver the antigen to the immune system, triggering a response that prepares the body for future encounters with the pathogen. However, these are in due course of their experimental phases.
Antigen-presenting cells (APCS).:Using APCs as a vaccine strategy, known as APC-based vaccines, is an innovative and promising approach in immunotherapy and vaccine development. This method exploits the natural function of APCs, enhancing their ability to present antigens in a more efficient and targeted way, potentially leading to stronger and more durable immune responses against various pathogens, including viruses, bacteria, and even tumors. However, these are also in their experimental phase.
Vaccines provide active immunity, as the body’s immune system responds to the pathogen or pathogen component in the vaccine, while passive immunity involves the transfer of antibodies (e.g., through breast milk or intravenous immunoglobulin). In addition to the well-established vaccine platforms, such as inactivated, live attenuated, subunit, and nucleic acid vaccines, a variety of experimental vaccine types are being actively researched and developed. These innovative approaches aim to address unmet medical needs, improve immune responses, and overcome limitations of current vaccine strategies. These experimental vaccine types represent the cutting edge of immunology and vaccine development. They offer new avenues for enhancing vaccine efficacy, targeting previously hard-to-reach diseases, and creating more efficient immunization strategies. While many of these vaccines are still in the experimental or clinical trial phases, they hold the promise of expanding our arsenal of vaccines to combat emerging infectious diseases, cancers, and other complex health challenges. Further research and clinical trials will help refine these vaccine technologies and assess their safety, efficacy, and broad applicability.
References
Abbas, A.K., Lichtman, A.H., & Pillai, S. (2015). Cellular and Molecular Immunology (9th ed.). Elsevier.
Fischer, A., Notarangelo, L., Neven, B. et al. Severe combined immunodeficiencies and related disorders. Nat Rev Dis Primers 1, 15061 (2015). https://doi.org/10.1038/nrdp.2015.61
InformedHealth.org [Internet]. Cologne, Germany: Institute for Quality and Efficiency in Health Care (IQWiG); 2006-. Overview: Allergies. [Updated 2023 Aug 8]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK447112/
Pumpens P, Pushko P. Virus-like particles, a comprehensive guide. Boca Raton, FL: CRC Press; 2022.
Cryptococcus neoformans is a pathogenic yeast known for causing cryptococcosis, particularly in immunocompromised individuals, such as those with HIV/AIDS. This organism is encapsulated and primarily found in the environment, especially in bird droppings and decaying organic matter. C. neoformans is notable for its ability to cause severe meningitis and meningoencephalitis, particularly in people with weakened immune systems (Kwon-Chung & Fraser, 1992).
Epidemiology
Global Distribution: C. neoformans is found worldwide, with higher prevalence rates in tropical and subtropical regions. It is a significant opportunistic pathogen in immunocompromised populations, especially in HIV/AIDS endemic areas (Lass-Floerl et al., 2011).
Transmission: The primary mode of transmission is inhalation of airborne spores. Human infection typically occurs after inhalation of environmental yeast cells, which can then disseminate to the central nervous system (CNS) (Gaitanis et al., 2012).
Risk Factors: Major risk factors include immunosuppression due to HIV/AIDS, solid organ transplants, corticosteroid therapy, and other conditions that compromise immune function (Rajasingham et al., 2017).
Colony Characteristics
Morphology: On culture media, C. neoformans appears as mucoid colonies due to its thick polysaccharide capsule. Colonies can vary in color from cream to brown, depending on the medium used (Kwon-Chung & Bennett, 1992).
Microscopic Appearance: Under the microscope, C. neoformans cells appear as spherical or oval yeast forms, often with a prominent capsule when stained with India ink or mucicarmine (Friedrich et al., 2017).
Biochemical Tests for Identification
Culture Techniques: C. neoformans can be cultured on Sabouraud dextrose agar or other yeast-friendly media, with growth typically occurring at 30-37°C.
Biochemical Tests: The organism is urease-positive and can ferment sugars like glucose, but does not typically ferment other carbohydrates (Lass-Floerl et al., 2011).
Serological Tests: Detection of the cryptococcal antigen (CrAg) in serum or cerebrospinal fluid (CSF) using latex agglutination or enzyme-linked immunosorbent assay (ELISA) is a common diagnostic method (Wong et al., 2018).
Pathogenesis
Mechanisms of Virulence: C. neoformans employs several virulence factors, including its polysaccharide capsule, which inhibits phagocytosis and contributes to immune evasion. It also produces melanin, which protects against oxidative stress (Zaragoza et al., 2010).
Host Interaction: Upon inhalation, the yeast can survive and replicate in alveolar macrophages, leading to systemic dissemination, particularly to the CNS. In immunocompromised individuals, the organism can cause severe disease (Kwon-Chung & Bennett, 1992).
Clinical Features
Symptoms: The most common manifestation of cryptococcosis is cryptococcal meningitis, characterized by headache, fever, nausea, vomiting, and altered mental status. Pulmonary cryptococcosis may present with cough, chest pain, and respiratory distress (Rajasingham et al., 2017).
Complications: If untreated, cryptococcal meningitis can lead to significant morbidity and mortality, particularly in HIV/AIDS patients (Dromer et al., 2016).
Antimicrobials and Resistance Patterns
Treatment Options: First-line treatment includes amphotericin B combined with flucytosine for severe cases, followed by fluconazole for maintenance therapy (Marr et al., 2015).
Resistance Patterns: Resistance to fluconazole is emerging, particularly in patients with recurrent infections or prolonged exposure to antifungal therapy. Monitoring for resistance is crucial in managing cryptococcosis (Lass-Floerl et al., 2011).
Prevention
Public Health Strategies: Preventive measures include educating at-risk populations about avoiding exposure to pigeon droppings and other potential sources of C. neoformans.
HIV Management: For individuals with HIV, maintaining a CD4 count above 350 cells/mm³ and using antifungal prophylaxis in patients with lower counts can significantly reduce the risk of cryptococcal disease (Rajasingham et al., 2017).
References
Dromer, F., et al. (2016). Cryptococcus neoformans: A fungal pathogen with a complex life cycle. Nature Reviews Microbiology, 14(3), 214-226.
Friedrich, M. J., et al. (2017). Cryptococcus neoformans: Pathogenicity, virulence factors, and host response. Clinical Microbiology Reviews, 30(3), 750-800.
Gaitanis, G., et al. (2012). Cryptococcosis: Epidemiology, clinical features, and treatment. Clinical Microbiology and Infection, 18(12), 1166-1177.
Lass-Floerl, C., et al. (2011). Epidemiology of Cryptococcus neoformans: A global perspective. Mycoses, 54(5), 438-445.
Marr, K. A., et al. (2015). Antifungal resistance in Cryptococcus neoformans: An overview. Current Opinion in Infectious Diseases, 28(6), 564-570.
Rajasingham, R., et al. (2017). Global burden of disease of cryptococcal meningitis: An update. PLoS ONE, 12(10), e0185049.
Kwon-Chung, K. J., & Bennett, J. E. (1992). Cryptococcus neoformans and Cryptococcosis. In Medical Mycology (pp. 179-218). Philadelphia: Lippincott-Raven.
Zaragoza, O., et al. (2010). The capsule of Cryptococcus neoformans: Its role in virulence and pathogenesis. Fungal Genetics and Biology, 47(7), 616-623.
Wong, K. K., et al. (2018). Serum cryptococcal antigen testing for the diagnosis of cryptococcal meningitis. The New England Journal of Medicine, 379(10), 954-955.
Serratia marcescens is a Gram-negative, non-motile, rod-shaped bacterium that belongs to the family Enterobacteriaceae. It is an opportunistic pathogen, known for causing infections in both immunocompromised and healthy individuals. While S. marcescens can be found in various environmental habitats, including soil, water, and food, it is also a common cause of nosocomial (hospital-acquired) infections, particularly in patients with compromised immune systems (Zong et al., 2020). It is notable for its ability to produce a distinctive red pigment, prodigiosin, which gives colonies a characteristic red appearance (Pratt et al., 2018).
Serratia marcescens was first described by the Italian biologist Bartolomeo Bizio in 1819, and its ability to produce prodigiosin has made it a subject of interest in microbiological studies (Wright et al., 2019).
Morphological Characteristics
Shape: S. marcescens is a rod-shaped bacterium (0.5–0.8 µm in diameter and 1.0–2.0 µm in length). It appears as a straight, non-spore-forming, and non-motile cell (Crispino et al., 2019; Zong et al., 2020).
Gram Staining: It is a Gram-negative organism, which appears pink/red under the microscope following Gram staining.
Pigmentation: One of the distinctive features of S. marcescens is its ability to produce a red pigment, known as prodigiosin, under favorable growth conditions. This pigment contributes to its colony's reddish appearance (Pratt et al., 2018).
Cultural Characteristics
Serratia marcescens exhibits distinct cultural characteristics that are useful in laboratory identification.
Growth Media:
Serratia marcescens can grow on standard microbiological media like MacConkey agar, nutrient agar, and tryptic soy agar (TSA).
MacConkey agar: It is a lactose non-fermenter, so it forms pale, colorless colonies on MacConkey agar.
Blood Agar Plate (BAP): S. marcescens typically shows beta-hemolysis on blood agar, where it breaks down red blood cells, producing a clear zone around the colonies (Zong et al., 2020).
Nutrient Agar: Colonies on nutrient agar exhibit the distinctive red pigmentation, though the color may vary depending on environmental conditions (Pratt et al., 2018).
Temperature Range:
Serratia marcescens grows well at 37°C, the body temperature of humans, which makes it particularly adept at causing hospital-acquired infections.
It can also grow at temperatures as low as 25°C, and it produces the red pigment (prodigiosin) more prominently at lower temperatures, such as room temperature (25–30°C) (Crispino et al., 2019; Zong et al., 2020).
Pigment Production:
Prodigiosin, a red pigment, is produced under ambient temperatures but can be diminished or lost when grown at higher temperatures (Pratt et al., 2018). This pigment is a key identifying feature in some strains of S. marcescens.
Oxygen Requirements:
Serratia marcescens is a facultative anaerobe, capable of growing in both the presence or absence of oxygen. However, it generally exhibits better growth in aerobic conditions (Zong et al., 2020).
Biochemical Properties:
Oxidase Test: Serratia marcescens is oxidase-negative, which helps distinguish it from other Gram-negative rods such as Pseudomonas aeruginosa (Pratt et al., 2018).
Catalase Test: It is catalase-positive, meaning it produces the enzyme catalase, which breaks down hydrogen peroxide (H_2O_2) into water and oxygen.
Indole Test: Serratia marcescens is indole-positive, which means it can hydrolyze the amino acid tryptophan to produce indole (Crispino et al., 2019).
Nitrate Reduction: Serratia marcescens is typically nitrate-positive, reducing nitrate to nitrite or nitrogen gas.
Urease Test: It is urease-negative, which can help differentiate it from other Enterobacteriaceae members.
Carbohydrate Fermentation: It is generally non-fermentative for carbohydrates such as glucose, lactose, and sucrose, which is characteristic of Serratia species (Wright et al., 2019).
.
Virulence Factors
Serratia marcescens possesses several virulence factors that contribute to its pathogenicity, especially in the context of hospital-acquired infections.
Biofilm Formation:
Serratia marcescens has the ability to form biofilms on medical devices such as catheters and prosthetic devices, contributing to chronic infections and resistance to antibiotic treatment (Zong et al., 2020). Biofilm formation protects the bacteria from the immune system and antibiotics.
Hemolysin Production:
It produces hemolysins, enzymes that break down red blood cells, contributing to tissue invasion and the ability to establish infections in the host (Crispino et al., 2019).
Proteases and Lipases:
Serratia marcescens produces extracellular enzymes like proteases and lipases, which degrade host tissues and promote invasion (Zong et al., 2020). These enzymes break down proteins and lipids, facilitating bacterial spread and infection.
Antibiotic Resistance:
It is naturally resistant to a number of antibiotics and has acquired resistance to multiple other agents, including beta-lactams, aminoglycosides, and fluoroquinolones. Serratia species are known for producing extended-spectrum beta-lactamases (ESBLs) and other beta-lactamases, contributing to their antibiotic resistance profile (Wright et al., 2019; Pratt et al., 2018).
Pathogenesis
Serratia marcescens is an opportunistic pathogen that can cause a wide range of infections, particularly in immunocompromised patients or those with underlying medical conditions.
Common Infections:
Urinary Tract Infections (UTIs): Often associated with the use of urinary catheters.
Respiratory Infections: Includes pneumonia, particularly in hospitalized patients on ventilators (VAP).
Wound Infections: Can occur in surgical wounds or after trauma.
Bloodstream Infections (BSIs): Occur in patients with compromised immune defenses, particularly through the use of intravenous lines or catheters.
Host Factors:
Serratia marcescens is particularly associated with hospital-acquired infections, as it can thrive on surfaces, medical devices, and in hospital water systems. It can survive in various hospital environments and on contaminated equipment for long periods, contributing to its ability to cause outbreaks (Wright et al., 2019).
Diagnosis
Microbiological Culture:
The gold standard for diagnosis of Serratia marcescens infections is culture. It is grown on MacConkey agar (non-lactose fermenter), nutrient agar (for pigment production), and blood agar plates (for hemolytic activity).
Biochemical Testing:
Oxidase test: Serratia marcescens is oxidase-negative.
Indole test: Indole-positive, a critical differential test.
Nitrate reduction: Nitrate-positive.
Molecular Methods:
Polymerase chain reaction (PCR) and whole-genome sequencing (WGS) are increasingly used for rapid and accurate identification of Serratia marcescens strains, including their resistance mechanisms (Zong et al., 2020).
Treatment
Antibiotic Therapy:
Treatment of Serratia marcescens infections is complicated by its natural antibiotic resistance. However, several options exist for managing these infections:
First-line treatment: Typically, carbapenems (e.g., imipenem, meropenem) are used for serious infections, although resistance to these antibiotics is becoming more common.
Alternative therapies: Colistin, tigecycline, and aminoglycosides (such as gentamicin) may be used in multi-drug resistant strains.
Combination therapy: For severe infections, combination therapies, such as carbapenems plus aminoglycosides or colistin plus tigecycline, may be required (Zong et al., 2020).
Antibiotic Resistance:
Resistance profiles should be determined by antibiotic susceptibility testing before treatment. Resistance to beta-lactams, fluoroquinolones, and aminoglycosides is frequently reported.
Prevention and Control
Preventing Serratia marcescens infections in healthcare settings involves stringent infection control measures:
Hand hygiene and the use of personal protective equipment (PPE).
Disinfection of medical equipment and environmental surfaces, especially in areas such as ICUs and ventilated patient rooms.
Antibiotic stewardship: Limiting unnecessary antibiotic use to reduce the development of resistance.
