Microbiology Exam 3 Flashcards

Primary molecular targets for antifungal agents are enzymes and other molecules involved in cell wall synthesis, plasma membrane synthesis, fungal DNA and protein synthesis, cellular function-related, and virulence factors.

Dermatophytes develop antifungal resistance through mechanisms such as altering drug targets, overexpressing efflux pumps, forming biofilms, enzymatic degradation of drugs, and modifying membrane composition, all of which reduce the efficacy of common antifungal treatments.

Mechanisms of antifungal drug resistance include reducing drug-target interactions (e.g., via drug affinity changes) and reducing intracellular drug levels (e.g., using drug pumps).

Specific events in virus replication identified as targets for antiviral agents are viral adsorption, penetration, uncoating, and viral nucleic acid synthesis as well as viral protein synthesis.

Antiviral drugs target five major areas: viral entry, uncoating, nucleic acid synthesis, assembly and release, and immune modulation, each disrupting different stages of the viral lifecycle to prevent infection and replication.

Amantadine targets the M2 ion channel of influenza A viruses to block viral uncoating, preventing the release of viral RNA into host cells, and is used to treat influenza A infections. Acyclovir is a nucleoside analog that inhibits viral DNA polymerase, causing premature termination of viral DNA replication, and is primarily used to treat herpesvirus infections such as herpes simplex and varicella-zoster. Rifampicin, though mainly an antibacterial for tuberculosis, has some antiviral effects by inhibiting RNA polymerase, though it is not commonly used against viruses in clinical settings.

Tamiflu (oseltamivir) is an antiviral medication used to treat and prevent influenza A and B. It works by inhibiting neuraminidase, an enzyme on the virus surface that helps release new viral particles from infected cells. By binding to and blocking this enzyme, Tamiflu prevents the spread of the virus within the host, reducing the severity and duration of flu symptoms. It is most effective when taken within the first 48 hours of symptom onset and can also be used prophylactically in high-risk situations to prevent infection.

Malaria is a life-threatening disease caused by Plasmodium parasites transmitted via female Anopheles mosquito bites. Antimalarial drugs target various parasite life cycle stages: erythrocytic (causing symptoms), liver (pre-symptomatic), and gametocytic (transmission). Common treatments include Chloroquine, which disrupts parasite hemoglobin digestion; Artemisinins, which generate toxic radicals; Atovaquone-Proguanil, which inhibits mitochondrial function; and Primaquine, targeting the liver stage to prevent relapses. These drugs are essential for both malaria treatment and prevention.

Chloroquine is used to treat malaria by interfering with the parasite's ability to digest hemoglobin, leading to toxic buildup and death of the parasite. Primaquine targets the dormant liver stage of Plasmodium vivax and P. ovale to prevent relapses by disrupting the parasite’s electron transport. Together, these drugs address different stages of the parasite lifecycle, aiding in comprehensive malaria treatment and prevention.

Trypanosomiasis, also known as sleeping sickness, is caused by the parasite Trypanosoma brucei, transmitted by tsetse flies. Drugs targeting this disease generally inhibit the parasite's unique metabolic pathways or structural components. For example, Pentamidine disrupts the parasite's mitochondrial function leading to death, while Suramin blocks enzymes essential for the parasite’s energy metabolism. Eflornithine, another key drug, specifically inhibits ornithine decarboxylase, an enzyme critical for the parasite's cell division and proliferation. Together, these drugs exploit specific vulnerabilities in the parasite's biology to treat trypanosomiasis effectively.

Pentamidine is an antiprotozoal medication used primarily to treat Trypanosoma brucei gambiense infection, which causes West African trypanosomiasis, also known as sleeping sickness. The drug targets the parasite by binding to its kinetoplast DNA (kDNA), disrupting essential biological processes such as DNA, RNA, and protein synthesis. This interference with the parasite's nuclear metabolism leads to its death, effectively treating the infection.

Giardia lamblia is a protozoan parasite that causes giardiasis, a diarrheal disease acquired mainly through contaminated water. The illness primarily affects the small intestine, leading to symptoms like diarrhea, abdominal cramps, and nausea. Treatment typically involves the drug metronidazole, which targets Giardia by entering the parasite's cells and disrupting its DNA structure. This action inhibits nucleic acid synthesis, effectively killing the parasite and resolving symptoms.

Metronidazole is used to treat bacterial and protozoal infections, including those caused by Giardia lamblia, which leads to giardiasis, a gastrointestinal disease characterized by diarrhea and abdominal discomfort. The drug operates by penetrating the cells of microorganisms and causing DNA damage. This disruption of DNA structure and function inhibits nucleic acid synthesis, ultimately leading to the death of the bacteria or protozoa. This mechanism makes metronidazole effective against anaerobic bacterial infections and protozoal diseases.

Toxoplasmosis is a disease caused by the parasite Toxoplasma gondii, which can infect most animals and birds, but primarily affects humans through contaminated food, soil, or contact with cat feces. The condition can be serious in pregnant women and immunocompromised individuals, leading to symptoms ranging from mild flu-like symptoms to severe neurological disorders. Treatment often involves a combination of pyrimethamine and sulfadiazine. Pyrimethamine inhibits folic acid synthesis in the parasite, crucial for its DNA synthesis and replication, while sulfadiazine interferes with the parasite’s ability to produce dihydropteroate, a compound necessary for folic acid production. Together, these drugs effectively halt the growth and replication of T. gondii in the host.

Pyrimethamine is an antiparasitic drug used primarily to treat toxoplasmosis and as part of intermittent preventive therapy for malaria. The drug targets the parasitic enzyme dihydrofolate reductase, which is essential for synthesizing folic acid, crucial for the parasite's nucleic acid and protein synthesis. By inhibiting this enzyme, pyrimethamine blocks the production of folic acid within the parasite, leading to impaired DNA synthesis and ultimately the death of the parasite. This specific targeting makes pyrimethamine an effective component in controlling the growth and spread of parasites in infected hosts.

Antibiotics target critical bacterial structures and processes: cell wall synthesis (e.g., penicillins disrupt enzymes building the cell wall, causing bacteria to lyse), protein synthesis (e.g., tetracyclines and macrolides inhibit ribosomes, stopping protein production), nucleic acid synthesis (e.g., fluoroquinolones inhibit DNA replication enzymes, rifampin blocks RNA polymerase), metabolic pathways (e.g., sulfonamides and trimethoprim disrupt folate synthesis, essential for bacterial growth), and cell membrane integrity (e.g., polymyxins increase membrane permeability, leading to cell death). These targets are specific to bacteria, minimizing damage to human cells.

target the 30S ribosomal subunit to inhibit protein synthesis, effective mainly against gram-negative bacteria.

inhibit cell wall synthesis, effective against both gram-positive and gram-negative bacteria, with multiple generations offering varying coverage.

bind to the 30S ribosomal subunit, inhibiting protein synthesis, effective against both types of bacteria.

beta-lactam antibiotics that inhibit cell wall synthesis, treating a broad range of infections.

inhibit folate synthesis, effective against both gram-positive and gram-negative bacteria.

inhibit DNA gyrase, affecting DNA replication, effective against both bacteria types.

inhibit the 50S ribosomal subunit, mainly effective against gram-positive bacteria.

inhibit cell wall synthesis, broad-spectrum coverage against both bacteria types.

inhibit the 50S ribosomal subunit, mainly targeting gram-positive bacteria.

inhibit cell wall synthesis, used mainly against gram-positive bacteria including MRSA.

Antibiotic resistance occurs when bacteria develop mechanisms to survive exposure to antibiotics, including genetic mutations that alter drug targets, the development of efflux pumps that expel antibiotics from the cell, enzymatic degradation which breaks down antibiotics, altered permeability to prevent antibiotics from entering the cell, and target modification to prevent antibiotics from binding effectively. These mechanisms can spread among bacteria via horizontal gene transfer, making infections harder to treat and often requiring higher doses or alternative medications.

Immunology is the study of the immune system, focusing on how the body defends itself against diseases through innate and adaptive immunity. Innate immunity provides immediate, non-specific protection via barriers like skin and immune cells such as phagocytes, while adaptive immunity involves specific responses from lymphocytes—B cells produce antibodies targeting specific antigens, and T cells destroy infected cells and regulate immune responses. The field also explores immunological memory, which speeds up responses to known pathogens, and issues like autoimmunity where the immune system attacks its own tissues, and allergies where it reacts to harmless substances. Immunology is fundamental to developing vaccinations, which activate the immune system to prevent disease without causing illness, and is crucial in areas like infectious diseases, oncology, and transplantation.

Chemokine receptor antagonists are drugs that block chemokine receptors on immune cells, thereby disrupting chemokine-mediated pathways and reducing inflammation. These antagonists are particularly useful in treating inflammatory and autoimmune diseases such as rheumatoid arthritis and multiple sclerosis by preventing the migration of inflammatory cells to sites of injury or inflammation. Additionally, they are employed in infectious disease treatment, as exemplified by maraviroc, which targets the CCR5 receptor used by HIV to enter and infect immune cells, thus helping to prevent HIV infection.

Fusion inhibitors are a class of antiviral drugs that prevent viruses from entering host cells by blocking the fusion of viral and host cell membranes. Specifically used in the treatment of HIV, drugs like Enfuvirtide target the gp41 protein on HIV-1, which is essential for the virus to merge its envelope with the host T-cell membrane. By binding to gp41, enfuvirtide inhibits the necessary conformational changes for fusion, effectively stopping viral entry and replication. This class of drugs is particularly valuable for managing HIV that is resistant to other antiretrovirals and is administered via injection, typically when other treatments are ineffective or inappropriate.

Reverse transcriptase inhibitors (RTIs) are antiviral drugs crucial for treating HIV by targeting the reverse transcriptase enzyme, which converts viral RNA into DNA, allowing the virus to integrate and replicate within the host. There are two types: nucleoside reverse transcriptase inhibitors (NRTIs), which mimic nucleotides causing premature DNA termination, and non-nucleoside reverse transcriptase inhibitors (NNRTIs), which bind directly to disrupt enzyme function. Used primarily in antiretroviral therapy, RTIs are combined with other antivirals to enhance efficacy and prevent resistance, effectively managing HIV infection and maintaining low viral loads.

Integrase inhibitors are antiretroviral drugs targeting the HIV integrase enzyme, essential for integrating viral DNA into the host genome, a crucial step in viral replication. By blocking this process, integrase inhibitors effectively halt HIV replication and progression. Common examples include Raltegravir, Elvitegravir, and Dolutegravir. These drugs are part of combination antiretroviral therapy, essential for reducing viral load, enhancing immune function, and minimizing resistance, making them highly effective in managing HIV infections.

Protease inhibitors (PIs) are a class of antiviral drugs used primarily to treat HIV by targeting the HIV protease enzyme, essential for viral maturation. By inhibiting this enzyme, protease inhibitors prevent the cleavage of polyproteins into functional units, resulting in the production of immature, non-infectious viral particles. This action reduces the viral load and prevents disease progression. Commonly used in highly active antiretroviral therapy (HAART) alongside other antiretrovirals, examples include Saquinavir, Ritonavir, and Lopinavir, with Ritonavir often used to boost the effectiveness of other PIs by increasing their levels in the blood.

Enveloped viruses have a lipid membrane with glycoproteins that aids in cell entry and exit through fusion, making them sensitive to environmental disruptors like detergents. Non-enveloped viruses lack this membrane, making them more robust and able to survive harsh conditions. They typically enter cells by endocytosis and exit by lysing the cell. The presence or absence of an envelope impacts their environmental stability and method of interacting with host cells.