Medical Microbiology Notes PDF
Document Details
Uploaded by FruitfulLime2736
2024
Tags
Summary
These notes cover various aspects of medical microbiology, including definitions of key terms, discussions of prokaryotes and bacterial structures, and an overview of other essential topics. This document is suitable for undergraduate-level study or anyone interested in learning more about microbiology.
Full Transcript
MEDICAL MICROBIOLOGY LEGEND ACTs: Artemisinin-based Combination Therapies AIDS: Acquired Immunodeficiency Syndrome HZV: Herpes Zoster Virus ATP: Adenosine Triphosphate LPS: Lipopolysaccharide CID: Cytomegalic Inclusion Disease MMR: Measles, Mumps, Rubella CJD...
MEDICAL MICROBIOLOGY LEGEND ACTs: Artemisinin-based Combination Therapies AIDS: Acquired Immunodeficiency Syndrome HZV: Herpes Zoster Virus ATP: Adenosine Triphosphate LPS: Lipopolysaccharide CID: Cytomegalic Inclusion Disease MMR: Measles, Mumps, Rubella CJD: Creutzfeldt-Jacob Disease NSAIDs: Nonsteroidal Anti-Inflammatory Drugs DNA: Deoxyribonucleic Acid PrP: Prior protein DPA: Dipicolinic Acid RNA: Ribonucleic Acid HBIG: Hepatitis B Immune Globulin RSV: Respiratory Syncytial Virus HBV: Hepatitis B Virus TSE: Transmissible Spongiform Encephalopathy HIV: Human Immunodeficiency Virus UTI: Urinary Tract Infection HSV: Herpes Simplex Virus 1 DEFINITIONS Pathogenicity: ability to cause disease in host organism Pathogenesis: process of disease development through various portals of entry Virulence: extent or degree of pathogenicity, where virulence factors (capsules, cell wall components, enzymes) ↑pathogenicity Host response: beneficial microorganisms living on/inside human body that prevent overgrowth of pathogenic microbes and produces useful substances e.g. vitamins; NOT harmful Innate immunity: host response/defense against infections from birth; rapid response; NO recognition or memory response Adaptive immunity: host response/defense against specific microbes; slow response; memory response PROKARYOTES Prenuclei (no nuclei) are unicellular microorganisms with peptidoglycan cell walls, that replicate by binary fission (single bacterium dividing into two equal cells) 2 BACTERIAL STRUCTURAL FEATURES Cell wall: Complex, semirigid structure that surrounds the cell (cytoplasmic) membrane and protects it from the outside environment by preventing bacterial cells from rupturing when the water pressure inside the cell is greater than that outside the cell (osmotic pressure) Plasma (cytoplasmic) membrane: Thin structure inside of the cell wall, enclosing the cytoplasm of the cell, consisting of primarily phospholipids, carbohydrates, and proteins – contains enzymes for metabolic reactions and has irregular infoldings called mesosomes caused by specimen preparation Image adapted from OpenStax College, Biology. Download for free at http://cnx.org/content/col11448/latest/ CELL WALL Teichoic acids primarily consist Consists of of alcohols and phosphates lipopolysaccharides (LPS) including lipid A (endotoxin) Image adapted from OpenStax College, Biology. Download for free at http://cnx.org/content/col11448/latest/ 3 BACTERIAL STRUCTURAL FEATURES EXTERNAL TO CELL WALL: Glycocalyx (sugar coat): substances that surround cells If substance is organized and firmly attached to cell wall, described as a capsule (protects pathogenic bacteria from phagocytosis) If substance is unorganized and loosely attached, described as slime layer Flagella: long, filamentous appendages to propel bacteria in various patterns of motility Fimbriae: occur at poles of the cell or distributed over entire surface; adhere to each other or surfaces (biofilm) Pili: longer than fimbriae (only one or two per cell), involved in motility and sometimes DNA transfer, also called conjugation (sex pili) GRAM STAINS Vibrio (short curved rod) Bacilli (rod) Gram-positive bacteria Purple or blue stains bind peptidoglycan cell walls Produce exotoxins (toxic proteins causing damage in small amounts) Gram-negative bacteria Pink or red stains Produce endotoxins (cell wall lipids causing pyrogenic response) Cocci (spherical) Images adapted from OpenStax College, Biology. Download for free at http://cnx.org/content/col11448/latest/ 4 ENDOTOXIN AND EXOTOXIN FEATURES EXOTOXIN ENDOTOXIN BACTERIAL Mainly gram-positive but can be gram-negative Gram-negative bacteria SOURCE bacteria Lipids, portions of LPS in outer CHEMISTRY AND Proteins, produced as part of growth and membrane of cell wall, that are RELATION TO metabolism, that are secreted into the liberated when bacteria die and BACTERIA surrounding medium during log phase the cell wall breaks apart Specific for a particular cell structure or function All produce the same symptoms, in the host (Many are enzymes that catalyze including chills, fever, weakness, EFFECTS biochemical reactions so a small amount is generalized aches, shock, death, harmful because they can act repeatedly) miscarriage ENDOTOXIN AND EXOTOXIN FEATURES EXOTOXIN ENDOTOXIN HEAT Unstable; can usually be destroyed at 60-80°C Stable; can withstand autoclaving STABILITY (except staphylococcal enterotoxin) (121°C for 1 hour) TOXICITY High Low LETHAL Small Considerably larger DOSE Gas gangrene, tetanus, botulism, diphtheria, Typhoid fever, urinary tract infections, DISEASES scarlet fever meningococcal meningitis 5 EXOTOXIN DISEASES Type of Exotoxin A-B Scalded skin Traveler’s Anthrax Botulism Tetanus Diphtheria Cholera syndrome diarrhea Enterotoxigenic Escherichia coli Bacillus Clostridium Clostridium Corynebacterium Staphylococcus Vibrio and Entero- anthracis botulinum tetani diphtheriae aureus cholerae aggregative E. coli EXOTOXIN DISEASES MEMBRANE- Type of DISRUPTING SUPERANTIGEN Exotoxin Gas gangrene and Antibiotic-associated Toxic Shock Food poisoning Syndrome (TSS) food poisoning diarrhea Clostridium perfringens and other species of Clostridium difficile Staphylococcus aureus Clostridium 6 BACTERIAL GROWTH PHASES Lag phase: the number of cells changes very little because the cells do not immediately reproduce in a new medium (little or no cell Stationary phase division) Number of cells (log) Log phase: cells begin to divide and logarithmically increase (most active) Log Death Stationary phase: growth rate slows, the (exponential) (decline) number of microbial deaths balances the phase phase number of new cells, and population stabilizes (equilibrium caused by exhaustion of nutrients, Lag phase waste products, or harmful changes) Death phase (logarithmic decline phase): Time number of deaths exceeds the number of new cells formed and the population is diminished OXYGEN REQUIREMENTS Type of bacteria? Description? Obligate aerobe Require O2 for growth Facultative anaerobe Aerobic bacteria that continue growing in absence of O2 Microaerophile Requires ↓[O2] to grow Capnophile Optimal growth at ↑[CO2] Aerotolerant anaerobe O2 NOT required for survival; NOT affected by O2 Obligate anaerobe Only grows in absence of O2 7 BACTERIAL IDENTIFICATION Staphylococci species may be coagulase- positive or -negative; Coagulase tests Staph aureus species are coagulase-positive Coagulase coagulate (clot) fibrinogen in blood Catalase tests Only in obligate aerobes and facultative anaerobes Hemolytic tests α-hemolytic produces distinctive greening; β-hemolytic presents clear Acid-fast stains Stains bacteria with cell walls of mycolic acid (waxy lipid) ATYPICAL BACTERIUM Rickettsia Obligate intracellular bacterium Transmitted by bites from ticks, mites, lice, etc. Chlamydia Obligate intracellular bacterium NO ATP metabolism Tetracycline-type or macrolide-type antibiotics Mycoplasma NO cell walls Tetracycline-type or macrolide- type antibiotics 8 Cell wall Cell membrane INHIBITORS OF CELL MEMBRANE FUNCTION DNA Isoniazid Amphotericin B THFA - Polymyxins INHIBITORS OF METABOLISM Sulfonamides mRNA PABA Trimethoprim Ribosome INHIBITORS OF NUCLEIC INHIBITORS OF CELL INHIBITORS OF PROTEIN ACID FUNCTION/SYNTHESIS WALL SYNTHESIS SYNTHESIS Fluoroquinolones Β-Lactams Tetracyclines Rifampin Vancomycin Aminoglycosides Daptomycin Macrolides Telavancin Clindamycin Fosfomycin Chloramphenicol Linezolid Figure 1: Classification of some antimicrobial agents by their sites of action. (THFA = tetrahydrofolic acid; PABA = p-aminobenzoic acid.) Ref: lippincot ANTIBIOTICS COVERAGE CHART: A SUMMARY 9 SEPSIS Systemic Inflammatory Response Syndrome (SIRS); referred to as “septicemia” referring to blood poisoning with pathogenic microorganisms or toxins Gram-negative bacteria (E. coli, Klebsiella pneumoniae) Likely cause of septic shock (↓BP is NOT controlled by fluid addition) Gram-positive bacteria (Staph. Aureus, MRSA, Strep. pneumoniae) Most common cause of sepsis Puerperal (Haemolytic streptococci) Gram-positive infection Nosocomial infection of uterus from birth or abortion Treatment includes fluids, supportive care and combination antibiotics: Vancomycin (not E. coli) plus Ceftriaxone or Piperacillin-tazobactam or Ciprofloxacin (for Pseudomonas) or Gentamicin (for Pseudomonas) BONE AND JOINT INFECTIONS Infection? Description? Pathogens? Treatment? Surgery and antibiotics Staph aureus, for at least 6 weeks Bone Osteomyelitis Gram-negative inflammation bacteria Joint IV antibiotics and fluid Arthritis Staphaureus inflammation drainage from joint Artificial body Empiric or targeted Prostheses parts Bacterial biofilm antibiotic therapy 10 GANGRENE Death of soft tissue due to loss of blood supply Treatment: hyperbaric Wounds cause blood Ischemia and necrosis chamber (preventing flow interruptions, occurs; Clostridium- clostridia growth), surgical and nutrient produced gases/toxins removal/ amputation of depletions play a role necrotic tissue, antibiotics GI INFECTIONS Infection? Description? Pathogens? Symptoms? Ingesting foods Staph aureus, Salmonella Food containing enterica, Clostridium N/V/D Poisoning enterotoxins perfringens Campylobacter jejuni, Inflammation of GI Salmonella enterica, N/D, abdominal Gastroenteritis tract Yersinia, Bacillus cereus, pain E. coli Colonic Antibiotic- V/D, abdominal associated inflammation after Clostridium difficile pain, bloody colitis extended-use of stools antibiotics 11 DYSENTERY Shigella species produces shiga virulent toxins causing Shigellosis (bacillary dysentery) presenting as severe diarrhea + blood or mucous General infection process of Shigella: 1. Attachment to M cells lining intestinal tract 2. Entrance into epithelial cells via membrane ruffle 3. Multiplication 4. Invasion of neighbouring epithelial cells while avoiding immune defenses 5. Formation of mucosal abscesses as epithelial cells are killed Note, M (microfold) cells are specialized epithelial cells of MALT and GALT (mucosa- and gut-associated lymphoid tissue) lining intestinal tract. TYPHOID FEVER Acute intestinal and systemic illness resulting from ingestion of foods contaminated by fecal-oral transmission of Salmonella enterica serotype Typhi bacteria Only in human feces; common in areas where sanitation is poor Multiply within phagocytic cells where lysed cells release bacteria systemically and into organs Symptoms include high fever, continuous headaches, diarrhea or constipation, abdominal pain, fatigue, loss of appetite, rash Pharmacologicaltreatment: chloramphenicol, fluoroquinolones, 3rd-gen cephalosporins Recovery from typhoid fever confers lifelong immunity Image adapted from OpenStax College, Biology. Download for free at http://cnx.org/content/col11448/latest/ 12 KERATITIS Inflammation of the cornea Not always infectious Non-infectious causes include minor injuries (e.g. foreign body in the eye, wearing contact lenses for prolonged periods of time) Infectious causes include bacteria (Pseudomonas aeruginosa, Staphylococcus aureus), viruses, fungi, and parasites May require treatment with anti-infective eye drops Referral is required to eye specialist to ensure no vision loss is present BRAIN ABSCESS Collection of infected material from local (e.g. ear infection) or remote (e.g. kidney) sources, within the brain Treatment requires both drainge and antimicrobial therapy: penicillin G, metronidazole, ceftriaxone Streptococcus viridians Staphylococcus aureus 13 LEPROSY Infecting pathogen: Mycobacterium leprae; prior name: Hansen’s disease 2 main forms reflect effectiveness of cell-mediated immune system Survives macrophage-ingestion; invades cells Nerve damage occurs from cell-mediated immune response Transmission: intimate and prolonged contact Non-contagious within few days IF treated with sulfone drugs Pharmacological therapy: dapsone (sulfone), rifampin and clofazimine (not available in Canada?); combination therapy commonly use Tuberculoid (neural) form: Loss of sensation in skin Lepromatous (progressive) form: surrounded by nodules Infected skin cells and disfigured nodules from all over body Occurs in people with effective Occurs in patients with least effective immune reactions immune reactions Progresses from tuberculoid stage unpredictably Recovery sometimes occurs spontaneously OTITIS, PHARYNGITIS, SINUSITIS Pharyngitis (strep Rhinosinusitis Otitis media Otitis externa throat) (sinusitis) Pathogens: Pathogens: Inflammation of Pathogens: S. S. pneumoniae, H. pharynx, tonsils, or pneumoniae, H. influenzae, Moraxella Pseudomonas nasophar ynx influenzae, catarrhalis aeruginosa, 1pathogens: VIRAL Moraxella catarrhalis Staphylococcus (children) aureus (common), GAS; Spontaneous Drug therapy: Neisseria gonorrhea Inflammation and/or resolution may Topical antibiotics and others are mucous thickening occur: “watchful (fluoroquinolones), unusual causes of ≥1 paranasal waiting” steroids, acidifying Drug therapy: sinuses agents (acetic acid) Supportive care in Drug therapy: Drug therapy: are mainstay of mild cases, “watchful Supportive care in Amoxicillin PO treatment; systemic waiting,” amoxicillin mild cases, “watchful therapy used in waiting,” amoxicillin severe cases 14 SCARLET FEVER Rash requires prior S. pyogenes exposure and occurs as delayed-type skin reaction to pyrogenic exotoxin (erythrogenic toxin); commonly occurs in association with pharyngitis thus patients often present with symptoms of strep throat as well Lysogeny: Viral reproduction characterized by integration of bacteriophage nucleic acid into host bacterium genome (or circular replicon in cytoplasm), where bacterium continues living and reproducing normally Pharmacological treatment is the SAME as streptococcal pharyngitis (NO additional therapy is required for skin rash) Toxin A converts nonvirulent Resulting symptoms of scarlet fever: rash, Bacteriophage T12 Streptococcus pyogenes raised carries speA gene (strep pyogenic bumps, peeling skin, exotoxin A bacterial strain into virulent red gene/scarlet fever toxin A gene) coding for erythrogenic toxin A strain through lysogeny spots tuning white when pressed LOWER RESPIRATORY TRACT INFECTIONS Pleurisy (infection of pleura) Many possible causes e.g. TB, bacterial infections (e.g. pneumonia), fungal or parasitic infections, autoimmune disorders Croup Contagious viral infection in patients presenting with common colds Hallmark symptom is barking cough due to swollen respiratory tract Pneumonia Bacterial or viral etiologies bacterial pathogen in CAP is Streptococcus pneumoniae Bronchitis (infection of bronchi) Majority of cases are viral; acute bronchitis is generally self-limiting 15 LOWER RESPIRATORY TRACT INFECTIONS Mycoplasma (Mollicutes) Causes pneumonia Treatment: macrolide or tetracycline Legionella (Legionella pneumophila) Causes Legionnaires’ disease (CAP) Treatment: fluoroquinolones, azithromycin Chlamydia (Chlamydia trachomatis) NO symptoms! Treatment: azithromycin (if C/I, use doxycycline) VIRUSES Obligate intracellular parasites replicate within hosts Contain either RNA or DNA genomes Capsid: protein shell Non-enveloped virus into animal cells occurs through endocytosis Enveloped virus into animal cells occurring through membrane fusion Bacteriophage into bacterial cells occurs through pores Image adapted from OpenStax College, Biology. Download for free at http://cnx.org/content/col11448/latest/ 16 BACTERIOPHAGE REPLICATION Image adapted from OpenStax College, Biology. Download for free at http://cnx.org/content/col11448/latest/ DIAGNOSTIC MICROBIOLOGY (VIROLOGY) Isolation (plaque method): bacteriophages in suspensions of bacteria in liquid media or cultures on solid media Identification: electron microscopy, Western blotting, ELISA, PCR Cultivation: cultivated in mice, rabbits, guinea pigs, embryonated eggs where cell cultures are growth mediums Images adapted from OpenStax College, Biology. Download for free at http://cnx.org/content/col11448/latest/ 17 VIRAL PATHOGENESIS Infection Productive Abortive Acute Latent Persistent Host response: apoptosis, immune response, autoimmunity VIRAL REPLICATION AND ANTIVIRAL DRUGS Step #1 VIRUS VIRUS Attachment and Uncoating penetration Cell Protein and nucleic acid synthesis Reverse transcriptase Genome integration Packaging and Viral Release VIRUS assembly Antiviral drugs different parts of viral replication process HSV and VSV infections: acyclovir, valacyclovir, famciclovir, penciclovir Cytomegalovirus (CMV) infections: ganciclovir, valganciclovir, cidofovir, foscarnet HIV: antiretroviral drugs 18 RESPIRATORY TRACT INFECTIONS: VIRAL CAUSES >200 different viruses e.g. rhinovirus, Common Cold coronavirus, adenovirus, respiratory syncytial virus (RSV) Upper respiratory tract infections Adenovirus, Epstein-Barr virus, Phar yngitis Cytomegalovirus, HSV Influenza virus A and B, parainfluenza Pneumonia virus, RSV (infant pneumonia) Lower respiratory tract infections Influenza (Flu) Influenza viruses A, B, and C CNS VIRAL INFECTIONS Disease? Virus? Description? Meningitis Enteroviruses More common than bacterial meningitis Causes paralysis; transmitted through Poliomyelitis Poliovirus types 1, 2, 3 ingestion of contaminated water Fatal encephalitis; transmitted by animal Rabies Rabies virus bites Arboviral encephalitis Arboviruses Active cases: chills, fever, HA 19 PRION DISEASES at io , na Chain reaction of protein l misfolding: new prions PrPsc ch an Infected brain tissue: porous g g spongiform degeneration Creutzfeldt-Jakob disease (CJD): rare, fatal transmissible Prion spongiform encephalopathy Nucleation Infection replication (TSE) Nucleation cycle Boiling and irradiation have PrPc no effect and routine Bre g autoclaving is not reliable rea PrP: prion protein ge ka in to p GI VIRAL INFECTIONS Mumps Mumps virus Hepatitis A Ingestion; immunoglobulin Parenteral, sexual contact; entecavir, lamivudine, Hepatitis B adefovir, tenofovir Hepatitis Parenteral; sofosbuvir, dasabuvir, + Hepatitis C (inflammation of ribavirin liver) Hepatitis D Parenteral + HBV co-infection; none Hepatitis E Ingestion; none Hepatitis F Parenteral; none Hepatitis G Parenteral; none Rotavirus Gastroenteritis (stomach flu) Norovirus Legend: transmission, treatment 20 MMR VIRAL INFECTIONS Measles Symptoms: resemble common cold + macular rash Transmission: respiratory droplets Harmful to immunocompromised (e.g. infants) and those who are not immunized Mumps Inflammation of parotid glands Transmission: saliva and respiratory secretions/droplets Rubella (German measles) Milder than measles; recovery confers immunity Symptoms: macular rash with small red spots + fever Transmission: respiratory droplets VIRAL INFECTIONS: HEPATITIS Virus Transmission Treatment Hepatitis A Ingestion Hep A Immune Globulin Hep B Immune Globulin Hepatitis B Parenteral; sexual contact Entecavir, lamivudine, adefovir, tenofovir Hepatitis C Parenteral Parenteral + Sofosbuvir, dasabuvir, ribavirin co-infection Hepatitis D None with HBV Hepatitis E Ingestion None Hepatitis F Parenteral None Hepatitis G Parenteral None 21 FETAL, NEWBORN, AND INFANT INFECTIONS Condition? Treatment? HIV: trans-placental infection of fetus or breast- Nucleoside reverse transcriptase milk inhibitors (NRTI) Cytomegalovirus: cytomegalic inclusion disease (CID) in newborns, placental transfer or through Ganciclovir and fomivirsen breastmilk Neonatal herpes: transfer through cross- placental barrier causing spontaneous abortion Acyclovir IV or and fatal damage Hepatitis B: mother considered chronic carrier Prevented with Hepatitis B Immune and transfer virus through breastmilk Globulin (HBIG) SKIN INFECTIONS Infection, virus? Description? Smallpox: smallpox virus 2 forms: variola major minor; respiratory transmission Measles: measles virus Respiratory transmission Rubella: rubella virus Respiratory transmission Genital herpes: HSV Direct contact transmission Chickenpox/shingles: VZV, HZ Respiratory transmission Warts: papillomavirus Direct contact transmission: treatment includes cryotherapy, electrodessication, laser Mild, common childhood disease; symptoms Roseola (6th disease): HHV-6,-7 include high fever and rash Similar to mild influenza +distinctive “slapped- 5th disease: Human parvovirus B19 cheek” facial rash 22 YELLOW FEVER Classic viral hemorrhagic fever Caused by genus flavivirus Transmitted by the mosquito, Aedes aegypti Early stage of severe cases: fever, chills, headache, nausea, vomiting Second stage: jaundice, yellowing skin that reflects liver damage INFECTIOUS MONONUCLEOSIS MONO or “kissing disease” Mononucleosis refers to lymphocytes with unusual lobed nuclei that proliferate in blood during acute infection Caused by Epstein-Barr virus Virus maintains persistent infection in mouth and throat Transmitted by direct contact, transfer of saliva or sharing drinking vessels Recovery is usually complete in a few weeks and immunity is permanent 23 VIRAL INFECTIONS Conjunctivitis: inflammation of conjunctiva Keratoconjunctivitis: inflammation of conjunctiva and cornea Caused by viruses that cause common cold Most common symptoms include redness, watery discharge, and burning, sandy, or gritty feeling in one eye Transmitted by direct contact Bacterial causes Transmitted by direct contact Bilateral ocular discharge, crusting, redness, itching ANTIVIRAL AGENTS Acyclovir, ganciclovir, penciclovir, ribavirin, lamivudine, foscarnet Primarily herpesviruses Nucleoside and Cidofovir Cytomegalovirus, possibly smallpox nucleotide analogs Adefovir dipivoxil Lamivudine-resistant infections Attachment and Zanamivir, oseltamivir Treatment of influenza uncoating Amantadine, rimantadine Treatment of influenza Amantadine, rimantadine Treatment of influenza Interferons Alpha interferon Viral hepatitis 24 PROTOZOAN DISEASES Protozoans are unicellular, eukaryotic organisms Protozoan diseases: African trypanosomiasis, amebiasis, amebic dysentery, Chagas’ disease, cryptosporidiosis, malaria, meningoencephalitis, toxoplasmosis, trichomoniasis Diiodohydroxyquinoline Amebic infections; amebicidal Malaria; effective against red Chloroquine Anti-protozoal blood cell stage only drug therapy Giardiasis, amebiasis, Metronidazole, Tinidazole trichomoniasis Nitazoxanide Giardiasis ECTOPARASITES Ticks (Dermacentor) Rocky mountain spotted fever ARACHNIDA Ticks (Ixodes) Lyme disease, babesiosis, ehrlichiosis Ticks (Ornithodorus) Relapsing fever Mites (Sarcoptes scabiei) Scabies Pediculosis; head (capitis) lice, INSECTA Lice (Pediculus humanus) body (corporis) lice Legend: class, genus, disease 25 MYCOLOGY Mycology is scientific study of fungi, eukaryotes with membrane-bound nuclei and many membrane-bound organelles Thick, rigid wall containing complex polysaccharides (chitin and glucans) Plasma membrane stabilized by ergosterol Replication is asexual or sexual or both, depending on species Most fungi produce spores in both sexual and asexual reproduction Asexual reproduction by fragmentation, budding, or producing spores Transmission to hosts by direct contact, ingestion, or respiratory route CANDIDA Candida albicans is a yeast-like opportunistic pathogen Opportunistic pathogens normally HARMLESS and become pathogenic Overgrowth of target pathogen = superinfection Cause? Infection? Treatment? ∆pH Vulvovaginal candiasis Miconazole Thrush Clotrimazole Host immune defenses Normal population altered Caspofungin causing overgrowth 26 ASPERGILLUS Genus of ubiquitous, filamentous fungi acting as opportunistic pathogens AIRBORNE INFECTION TREATMENT Affects Caspofungin immunocompromised Eye or lung infection (Cancidas), member patients e.g. cancer, Aflatoxin poisoning of echinocandin lung disease by mycotoxin group Transmission: produced by fungi causing hepatic Voriconazole, inhalation of member of triazole Aspergillus spores cancer and cirrhosis group (conidia) HISTOPLASMOSIS pathogen: Histoplasma capsulatum Soil reservoir Transmission: inhalation of airborne conidia infection: pulmonary (may spread) Infection Amphotericin B (mod-severe), itraconazole Treatment (mild-mod), fluconazole 27 BLASTOMYCOSIS SOIL RESERVOIR Blastomyces 1 infection: pulmonary, and rapidly dermatitidis spreads causing cutaneous ulcers Often mimics other disease states INFECTION Mostly asymptomatic Starts in lungs Note: Blastomycosis usually known as resembling North American blastomycosis to bacterial differentiate it from South American pneumonia blastomycosis TREATMENT Amphotericin B, itraconazole COCCIDIOIDOMYCOSIS Fungal pulmonary disease caused by Coccidioides immitis Reproduction: form airborne arthroconidia (carried through wind) that are inhaled Endospore: specialized “resting” cell containing dipicolinic acid (DPA) which products endospore DNA against damage Symptoms: chest pain, fever, coughing, weight loss Treatmet: imidazole drugs, amphotericin B (severe) 28 CRYPTOCOCCOSIS Also known as Cryptococcus neoformans meningitis 1 pathogens: Cryptococcus neoformans and C. grubii Transmission: inhalation of dried, bird droppings and soil with spores Form spherical cells resembling yeasts, reproduce by budding, and produce extremely heavy polysaccharide capsules Treatment: combination of amphotericin B and flucytosine DERMATOPHYTES Ringworm Only affect epidermis, hair and nails Infections are called dermatomycoses or cutaneous mycoses Trichophyton infects hair, skin or nails Microsporum infects hair or skin Epidermophyton infects skin and nails Disease? Location? Treatment? Scalp Oral antibiotic, griseofulvin Tinea capitis Tinea pedis Feet Topical terbinafine or butenavine Tinea Oral itraconazole and terbinafine Nails unguium Tinea Miconazole and clotrimazole Groin cruris Image adapted from OpenStax College, Biology. Download for free at http://cnx.org/content/col11448/latest/ 29 Endoplasmic reticulum (inhibit ergosterol synthesis) Imidazoles Triazoles Nucleus Mitotic spindle Griseofulvin Cell wall Echinocandins DNA synthesis Plasma membrane Flucytosine Polyenes (amphotericin B) ANTIFUNGAL AGENTS Polyenes Amphotericin B Clotrimazole, miconazole MOAL: fungal sterols Azoles Ketoconazole (plasma membrane) Voriconazole Allylamines Terbinafine MOAL: fungal cell walls Echinocandins Caspofungin MOAL: nucleic acid Flucytosine inhibition Griseofulvin Other antifungals Tolnaftate 30 HOSPITAL EPIDEMIOLOGY 1 Study of occurrence, distribution, and determinants of health and disease in a hospital. Data collection of disease and tracking spread to identify mode of transmission 2 Information from clinical records, patient interviews, and surveillance. 3 Nosocomial infections:. hospital-acquired Case reporting: Descriptive report disease to epidemiology: collect datadisease health officials describing Experimental Analytical epidemiology: epidemiology: analyze data to determine perform experiments to test hypothesis cause CAUSE OF NOSOCOMIAL INFECTIONS Microorganism in hospital environment Potential pathogens: Staphylococcus aureus Enterococcus Compromised status of host E. coli P. aeruginosa Enterobacter Breaking chain of transmission in hospital Klebsiella pneumoniae Clostridium difficile 31 CHANGE LOG September 2023 Content reviewed; no changes made March 2024 Significant changes made throughout April 2024 Slides 40, 42: Updated agents used in hepatitis B July 2024 Content reviewed; minor formatting changes made 32