Lecture 8: Microbial Diseases of Respiratory System PDF

LECTURE 8: MICROBIAL DISEASES OF RESPIRATORY SYSTEM [MICRO 20] MICROBIOLOGY FOR NURSING UP College of Nursing 2027 PROFESSOR/INSTRUCTOR: GERALDINE B. DAYRIT, RMT, MSc, DRDM, RMicro, PhD [TRANS] UNIT 8: MICROBIAL D...

LECTURE 8: MICROBIAL DISEASES OF RESPIRATORY SYSTEM [MICRO 20] MICROBIOLOGY FOR NURSING UP College of Nursing 2027 PROFESSOR/INSTRUCTOR: GERALDINE B. DAYRIT, RMT, MSc, DRDM, RMicro, PhD [TRANS] UNIT 8: MICROBIAL DISEASES OF RESPIRATORY SYSTEM NON-SPECIFIC SYMPTOMS 10 OUTLINE SYMPTOMS OF URT INFECTIONS 10 THE RESPIRATORY SYSTEM 2 DIAGNOSIS OF URT 10 RESPIRATORY TRACT INFECTIONS 2 TREATMENTS OF URT 10 UPPER RESPIRATORY TRACT INFECTIONS (URIs) 2 SUMMARY OF URT INFECTIONS 10 LOWER RESPIRATORY TRACT INFECTIONS (LRIs) 2 HUMAN RHINOVIRUS (HRV) 10 PATHOGENESIS 2 TRANSMISSION OF RHINOVIRUS 11 BACTERIAL PATHOGENESIS 2 PATHWAY OF RHINOVIRUS 11 VIRAL PATHOGENESIS 3 IMMUNOLOGIC RESPONSE OF HOST TO RHINOVIRUS 12 STREP THROAT 3 WHO ARE INFECTED? 12 DEFINING CHARACTERISTICS OF S. PYOGENES 3 SYMPTOMS OF RHINOVIRUS 12 PYRROLIDONYL ARYLAMIDASE POSITIVE 3 DIAGNOSIS OF RHINOVIRUS 12 CULTIVATION 3 TREATMENTS OF RHINOVIRUS 13 BACITRACIN TEST 3 SUMMARY OF RHINOVIRUS 13 VIRULENCE FACTORS 3 PNEUMONIA 13 SYSTEMIC ASPECTS OF S. PYOGENES 4 PNEUMONIA CATEGORIES 14 MODE OF TRANSMISSION AND AFFECTED POPULATIONS 4 STAGES 14 ASSOCIATED MORBIDITIES 4 SYMPTOMS 14 POST-INFECTIOUS SEQUELAE 5 DIAGNOSIS 14 ACUTE RHEUMATIC FEVER 5 TREATMENT 14 POST-STREPTOCOCCAL GLOMERULONEPHRITIS 5 MYCOPLASMA PNEUMONIAE 14 SYMPTOMS 5 PATHWAY OF PATHOGENS IN MYCOPLASMA DIAGNOSIS 5 PNEUMONIA 15 TREATMENT 6 SYMPTOMS 15 RECAP 6 DIAGNOSIS 15 DIPHTHERIAE 6 TREATMENT 15 DEFINING CHARACTERISTICS OF S. PYOGENES 6 PERTUSSIS 16 DIPHTHERIA TOXINS (DT) 6 TRANSMISSION 16 MODE OF TRANSMISSION 7 MECHANISM 16 COMPLICATIONS 7 BORDETELLA PERTUSSIS 16 SYMPTOMS 7 PERTUSSIS INFECTION 16 DIAGNOSIS 7 DIAGNOSIS 16 TREATMENT 7 TREATMENT 16 RECAP 8 PERTUSSIS VACCINE 16 UPPER RESPIRATORY TRACT INFECTIONS 8 COMMUNITY ACQUIRED PNEUMONIA 17 PATHWAY OF AIR IN THE UPPER RESPIRATORY TRACT 8 TRANSMISSION 17 NASAL CAVITY 8 H. INFLUENZAE TYPE B 17 PARANASAL SINUSES 8 H. INFLUENZAE NONTYPABLE 17 PHARYNX (THROAT) AND LARYNX (VOICEBOX) 8 MECHANISM 17 TRACHEA AND LUNGS 8 HAEMOPHILUS INFLUENZAE 17 OTHER PARTICLES WE BREATHE (OTHER THAN AIR) 9 CULTIVATION 17 PATHWAY OF PATHOGENS IN URT INFECTIONS 9 ENCAPSULATED HAEMOPHILUS INFLUENZAE 17 TYPES OF UPPER RESPIRATORY INFECTIONS 9 NONENCAPSULATED HAEMOPHILUS INFLUENZAE 17 RHINITIS 9 BOTH ENCAPSULATED AND UNCAPSULATED 17 PHARYNGITIS 9 SYMPTOMS 18 LARYNGITIS 10 H. INFLUENZAE TYPE B 18 CLINICAL MANIFESTATIONS OF URT INFECTIONS 10 H. INFLUENZAE NONTYPABLE 18 DIAGNOSIS 18 TRANSCRIBERS: CORPUZ, LLANTERO, LOQUIAS, PESIGAN, VERA | EDITOR: LEJANO PROOFREADER: LEJANO ACADEMICS AND RESEARCH COMMITTEE 1  TRANS 8: MICROBIAL DISEASES OF RESPIRATORY SYSTEM TREATMENT 18 Can be caused mostly by viruses H. INFLUENZAE TYPE B 18 ○ Can also be caused by bacteria and fungus some H. INFLUENZAE NONTYPABLE 18 times LEGIONELLA PNEUMOPHILA 18 LEGIONELLOSIS 19 UPPER RESPIRATORY TRACT INFECTIONS (URIs) THIN PEPTIDOGLYCAN 19 Most common of all communicable diseases NON-SPORE FORMING AEROBIC 19 Transmitted from one person to another by airborne FACULTATIVE INTRACELLULAR 19 droplets spread via coughing or sneezing OXIDASE & CATALASE POSITIVE 19 Include: GROW ON BUFFERED CHARCOAL YEAST EXTRACT ○ Self-limiting infections (BCYE) 19 E.g., Rhinitis (common cold) TRANSMISSION 19 ○ More severe acute infections in the ear and DIAGNOSIS 20 pharynx TREATMENT 20 E.g., Acute otitis media, Pharyngitis RECAP 20 INFLUENZA 21 LOWER RESPIRATORY TRACT INFECTIONS (LRIs) MODE OF TRANSMISSION 21 SYMPTOMS 22 Affect the airways, mainly the bronchi and lungs COMPLICATIONS 22 Inflammation of the airways or pulmonary tissue DIAGNOSIS 23 Common LRIs RAPID INFLUENZA DIAGNOSTIC TEST 23 ○ Croup VIRAL CULTURE 23 ○ Chronic Bronchitis POLYMERASE CHAIN REACTION 23 ○ Pneumonia TREATMENT 23 ○ Pulmonary Tuberculosis PREVENTION - VACCINATION 23 Contagious bacterial infection involving TRIVALENT INACTIVATED INFLUENZA VACCINE (TIV) 23 the lungs LIVE ATTENUATED INFLUENZA VACCINE (LAIV) 23 VACCINATION - RISKS 23 PATHOGENESIS FLU VACCINE 24 REDUCES RISK BY HALF 24 BACTERIAL PATHOGENESIS FACTORS OF EFFECTIVENESS 24 VACCINATION EVERY YEAR 24 SUMMARY 24 DIFFUSE PNEUMONIA 24 PATHOLOGY AND CAUSES 25 DIAGNOSIS 25 THE RESPIRATORY SYSTEM Comprised of the organs that enable breathing Mechanism ○ Air enters the nostrils and mouth, followed by the pharynx (throat) and larynx (voice box), which lead to the trachea (windpipe) ○ In the thoracic cavity, the trachea splits into two bronchi that allow air to enter the lungs ○ The bronchi split into progressively smaller bronchioles and terminate in small groups of tiny sacs in the lungs called alveoli, where gas exchange occurs RESPIRATORY TRACT INFECTIONS Very common infections in the conditions of (1) changing weather, (2) environmental or host health conditions, which cause infection of sinuses, throat, and lungs TRANSCRIBERS: CORPUZ, LLANTERO, LOQUIAS, PESIGAN, VERA | EDITOR: LEJANO PROOFREADER: LEJANO ACADEMICS AND RESEARCH COMMITTEE 2  TRANS 8: MICROBIAL DISEASES OF RESPIRATORY SYSTEM VIRAL PATHOGENESIS ○ Small sample of the species is inoculated to a disk pad that is embedded with Pyrrolidonyl Beta Naphthylamide STREP THROAT Mechanism: Pathogen: Streptococcus pyogenes ○ L-Pyrrolidonyl Arylamidase hydrolyzes to ○ Sometimes called “Strep pyogenes” or “Group A Pyrrolidonyl Beta Naphthylamide to produce Strep” (Lancefield Classification) Beta-Naphthylamide Lancefield classification is developed by ○ Beta-Naphthylamide is then added with Rebecca Lancefield N-Methylaminocinnamaldehyde ○ Etiology ○ Results in bright red color that confirms S. “Strepto” → chain pyogenes is indeed Pyrrolidonyl Arylamidase “Coccus” → round positive “Pyo” → pus “Genes” → forming CULTIVATION ○ Round bacteria that grow in chains When cultivated in a Blood Agar, Strep pyogenes colonies DEFINING CHARACTERISTICS OF S. PYOGENES cause Beta-Hemolysis (also known as Complete Hemolysis) GENERAL UNIQUE This is because Strep pyogenes produce chemicals called CHARACTERISTICS CHARACTERISTICS “Streptolysins” (UNLIKE OTHER COMMON ○ These chemicals hydrolyze Hgb to transparent, COCCI) yellow-colored byproducts Thick Peptidoglycan Cell Pyrrolidonyl Arylamidase BACITRACIN TEST Wall (Gram-Positive) Positive Other Streptococcus species, such as S. agalactiae, are Non-motile Cultivation and also hemolytic Beta-Hemolysis ○ Therefore, Bacitracin Test is also done to further differentiate S. pyogenes No Spores Bacitracin Test Mechanism: ○ A disk of Bacitracin is added to the Blood Agar Facultative Anaerobe (can Other Virulence Factors ○ S. pyogenes is bacitracin sensitive, hence the survive in aerobic and colonies die off anaerobic conditions) In S. agalactiae, colonies remain intact upon the addition of bacitracin Catalase Negative (does not make enzyme catalase) VIRULENCE FACTORS PYRROLIDONYL ARYLAMIDASE POSITIVE Salt weaponry that help attack and destroy the host cells, and evade the immune system Makes the enzyme “L-Pyrrolidonyl Arylamidase” Overview of the test: TRANSCRIBERS: CORPUZ, LLANTERO, LOQUIAS, PESIGAN, VERA | EDITOR: LEJANO PROOFREADER: LEJANO ACADEMICS AND RESEARCH COMMITTEE 3  TRANS 8: MICROBIAL DISEASES OF RESPIRATORY SYSTEM TOXIC SHOCK VIRULENCE DESCRIPTION SYNDROME, which FACTOR triggers widespread systemic vasodilation, Encapsulated Covered by polysaccharide layer called making BP drop hence capsule leading to poor organ perfusion Adherence Lipoteichoic Acid Increases hemolysis in dermal Proteins and submucosal blood capillaries Streptococcus Fibronectin Binding protein (SfbI) SYSTEMIC ASPECTS OF S. PYOGENES M Protein (helps S. pyogenes to attach to From the bloodstream, S. pyogenes can spread to: the skin or pharyngeal mucosa) ○ Lungs Pneumonia Toxins Hyaluronidase Lung Abscesses Destroys hyaluronic acid, which ○ Heart keeps cells of the connective Form clumps or vegetations in the heart tissues and vessels tightly linked valves Destruction of hyaluronic acid Infective Endocarditis results in: ○ Central Nervous System ○ Local inflammation Brain Abscess ○ Enables bacteria to Meningitis spread to the Despite its harm, S. pyogenes can cause no harm and bloodstream peacefully colonize the (1) skin, (2) mucosa of pharynx or throat, (3) vagina, and (4) rectum Streptolysin O and S ○ These are regulated by the immune system, In the bloodstream, Streptolysin which restricts growth and prevents spread O and S are utilized by the pathogen for hemolysis or RBC destruction MODE OF TRANSMISSION AND AFFECTED POPULATIONS Streptococcal Pyrogenic Exotoxins SpcA, SpcB, and SpcC The pathogen gets to the bloodstream via SpcA and SpcC are ○ Breach on skin superantigens ○ Mucosal laceration ○ Don’t need to to be ○ Post-surgery “eaten up” and Problems arise in immunocompromised and/or processed by immunocompetent individuals such as: antigen-presenting cells ○ Infants and elderly to generate an immune ○ HIV-infected populations response from T-cells ○ Diabetic patients ○ Interact immediately ○ Malignancy with Class II MHC molecules on the ASSOCIATED MORBIDITIES surface of the macrophage DISEASE DESCRIPTION ○ This forms a superantigen MHC Strep Throat Inflammation of the pharyngeal complex,which interact mucosa and tonsils and stimula ~30% of entire T-cell population Scarlet Fever Associated with Strep Throat ○ Causes CYTOKINE Intracapillary hemolysis results in STORM, as it bright red skin rash stimulates the release of different inflammatory cytokines Impetigo S. pyogenes infects epidermis ○ The CYTOKINE Superficial skin lesions that look like STORM may result in honey clusters TRANSCRIBERS: CORPUZ, LLANTERO, LOQUIAS, PESIGAN, VERA | EDITOR: LEJANO PROOFREADER: LEJANO ACADEMICS AND RESEARCH COMMITTEE 4  TRANS 8: MICROBIAL DISEASES OF RESPIRATORY SYSTEM Erysipelas If the pathogen invades deeper, it can SYMPTOMS affect the upper dermis and superficial lymphatics Depend on the particular infection Cellulitis If it gets to the lower dermis, it causes Cellulitis DISEASE SYMPTOMS Acute, painful, quick-spreading infection of lower dermis and Pharyngitis Fever subcutaneous tissue Painful swallowing Reddish, swollen tonsils that may Necrotizing When it gets deeper to the muscle have pus Fasciitis fascia and subcutaneous tissue, the pathogen causes necrosis Impetigo Itchy honey-colored scabs which may be fluid-filled blisters POST-INFECTIOUS SEQUELAE Erysipelas Warm, painful lesions on the skin with raised edges Complications that arise even after elimination of the bacteria Strep Pharyngitis can cause complications such as: Cellulitis If it gets to the lower dermis, it causes ○ Acute Rheumatic Fever Cellulitis ○ Post-Streptococcal Glomerulonephritis Acute, painful, quick-spreading infection of lower dermis and ACUTE RHEUMATIC FEVER subcutaneous tissue Necrotizing Fever Arises because S. pyogenes has a bacterial M protein Fasciitis Painful and purple skin over affected ○ Mimics the structure of some proteins that make part up some body tissues such as Myosin Scarlet Fever Fever Glycogen of Heart Muscle Bright-red skin rash Smooth Muscle Cells Sandpaper feel on tongue ○ Not the same, but similar enough to let the immune system confuse these self-structures Acute Join Inflammation with the M protein Rheumatic Heart Damage ○ Results in Type II Sensitivity Reaction Fever ○ Resulting in new heart Increase in IgG and IgM antibodies murmurs which supposedly attack the M protein, Nodules but instead attacks own body structures ○ Typically seen in Myocarditis elbows, knees, and Infective Endocarditis forearms Pericarditis Erythema Marginatum ○ Rash with thick red POST-STREPTOCOCCAL GLOMERULONEPHRITIS margins Sydenham’s Chorea Acute inflammation of the kidney’s glomeruli ○ Rapid involuntary Often seen after impetigo movement of face and Typically seen 2-4 weeks after the initial infection due to hands Type III Sensitivity Reaction ○ Streptococcal Antigens that remain in blood Post-Streptoco Facial Edema combine with antibodies to form antigen-antibody ccal Dark Red Urine complexes Glomerulonep ○ Glomerular damage ○ These complexes are deposited in the basement hritis results in hematuria membrane of the glomerulus ○ Complement system is then activated, which attracts neutrophils to the glomeruli DIAGNOSIS ○ Results in kidney damage Rapid Strep Test (RST) ○ Bacterial antigens in throat swab TRANSCRIBERS: CORPUZ, LLANTERO, LOQUIAS, PESIGAN, VERA | EDITOR: LEJANO PROOFREADER: LEJANO ACADEMICS AND RESEARCH COMMITTEE 5  TRANS 8: MICROBIAL DISEASES OF RESPIRATORY SYSTEM ○ Gives a lot of false positives since Strep code for Diphtheria Toxin (DT) pyogenes can peacefully colonize the throat production Culture from Throat Swab Following this, Diphtheria may ○ Required for a definitive diagnosis occur Cultures from Blisters of Debrided Tissues Infection with a characteristic tough leathery membrane ○ Used for skin infections that forms in the pharynx Blood Cultures Greatly affects unvaccinated or immunocompromised ○ Used for systemic infections people TREATMENT DEFINING CHARACTERISTICS OF S. PYOGENES Penicillin (generally) ○ Pathogen does not exhibit sensitivity GENERAL CHARACTERISTICS Medications given to those allergic to Penicillin ○ Cephalosporins (Ceftriaxone) Thick Peptidoglycan Cell Wall (Gram-Positive) ○ Marolides (Azithromycin) Urgent Tissue Debridement Aerobic (requires oxygen to grow) ○ For Necrotizing Fasciitis No Spores RECAP When stained with Albert’s Stain: — Green — Metachromatic Granules: Dark blue spots made of phosphate at the bacterial poles — Pattern that resembles chinese letters when clustered together Fastidious — Only grow on nutrients-enriched media — Cystine-Tellurite Blood Agar: the usual media to allow its growth into black colonies DIPHTHERIA TOXINS (DT) Cytotoxic protein that causes damage to host cells Determines if a subspecies is toxigenic DIPHTHERIAE Has 2 main subunits—A and B—that are joined by a disulfide bond Pathogen: Corynebacterium diphtheriae ○ Each subunit plays a specific role in the invasion Etiology and destruction to the host’s cells ○ “Coryne” (Gk.) → club Mechanism: ○ “Diphtheriae” (Gk.) → leather ○ B-Subunit, the largest portion, functions to help Subspecies binding to the host cell membrane ○ Has 4 main subspecies ○ After attaching to the host cells, the DT complex C. diphtheriae mitis gets slowly engulfed by the cell membrane, which C. diphtheriae intermedius invaginates to form a sac on its inner side C. diphtheriae gravis ○ The sac then separates from the actual cell C. diphtheriae belfanti membrane forming a vesicle called an endosome ○ Can be toxigenic or non-toxigenic ○ Within the host cell cytoplasm, the medium inside Depending if they produce diphtheria the endosome becomes highly acidic toxin (DT) ○ As a consequence, the disulfide bonds holding ○ Mechanism the two subunits together becomes weak and All subspecies start out as non-toxigenic eventually breaks These become toxigenic after infection This occurrence separates the subunits by a beta-bacteriophage ○ The A-Subunit then diffuses through the Virus merges genome with that endosome membrane into the cytoplasm, where of the bacteria’s it goes straight to the ribosomes Has a genome that contains ○ Upon arrival to the ribosomes, the A-subunit tox-genes, which houses the interferes with cell protein synthesis TRANSCRIBERS: CORPUZ, LLANTERO, LOQUIAS, PESIGAN, VERA | EDITOR: LEJANO PROOFREADER: LEJANO ACADEMICS AND RESEARCH COMMITTEE 6  TRANS 8: MICROBIAL DISEASES OF RESPIRATORY SYSTEM This happens as the A-subunit contains an ADP ribose group, which attaches to SYMPTOMS the elongation factor (EF2), an important ribosomal protein that joins amino acids together during protein synthesis DISEASE SYMPTOMS ○ ADP Ribosylation Complete deactivation of EF2 stops General Low-grade fever protein synthesis, thereby resulting in Malaise and weakness cell death Pharyngeal Sore throat MODE OF TRANSMISSION Diphtheria Swollen neck (bull neck) Difficulty breathing r/t Via respiratory droplets (e.g., coughing and sneezing) pseudomembrane formation which result in PHARYNGEAL DIPHTHERIA Respiratory wheezes or stridor r/t Respiratory droplets enter the body via open lesions on pseudomembrane formation the skin which cause CUTANEOUS DIPHTHERIA Mechanism: Myocarditis Arrhythmias ○ C. diphtheriae attaches to the pharyngeal Heart failure epithelial cells, releasing DT toxin in the process ○ Heart cannot pump Causes local inflammation that leads to enough blood to meet necrosis and neck swelling the body’s demands ○ Necrotic tissue builds up in the pharynx or larynx, resulting in gray adherent, leathery Acute Tubular Oliguria — decreased urine membrane—commonly referred to as Necrosis production PSEUDOMEMBRANE In some cases, a portion of the Oculomotor Diplopia (double vision) pseudomembrane can detach and get Nerve Palsy Unable to move eyes up, down, lodged into the trachea or bronchi and/or to the side This can block the airways completely, resulting death by asphyxiation DIAGNOSIS COMPLICATIONS Culture If left untreated, C. diphtheriae gradually invades deeper ○ Culture of swabs from pharynx or suspected skin into the pharyngeal wall until it reaches the bloodstream, lesion to isolate C. diphtheria where it can move to other distant parts such as: ○ When culture test positive, the next step is to ○ Heart determine if the strain is toxigenic Myocarditis or inflammation of the heart Elek’s Test muscle ○ To determine is the strain from the positive ○ Kidneys culture test is toxigenic Acute Tubular Necrosis or destruction to ○ C. diphtheriae is grown on an agar plate the renal tubules embedded with antitoxin impregnated filter paper ○ Nerves ○ Mechanism Nerve Demyelination or destruction of If the strain makes DT, the toxin reacts the myelin sheath covering the axons with the antitoxin Leads to polyneuropathy Bands of visible precipitations are Affects the oculomotor nerve, resulting observed in OCULOMOTOR NERVE PALSY Polymerase Chain Reaction (PCR) Muscles that move the eye are ○ Detecting the bacteria’s toxigenicity in its DNA impaired ○ Phrenic Nerve TREATMENT Innervates the diaphragm May cause difficulty breathing Starts upon clinical suspicion, and even before diagnostic confirmation Treatment Plans ○ Isolate patient to prevent spread ○ Penicillin G is given Erythromycin in case of penicillin allergy ○ Diphtheria Antitoxin TRANSCRIBERS: CORPUZ, LLANTERO, LOQUIAS, PESIGAN, VERA | EDITOR: LEJANO PROOFREADER: LEJANO ACADEMICS AND RESEARCH COMMITTEE 7  TRANS 8: MICROBIAL DISEASES OF RESPIRATORY SYSTEM Given to counter the effects of bacterial mucus is salty, sticky, and contains toxin should the infecting bacteria be lysozymes which are enzymes that proven toxigenic with Elek’s Test help kill bacteria ○ Vaccine Nose hairs at the entrance of the nasal cavity get coated Consists of a Toxoid, a modified DT with that mucus and are able to trap large particles of dust, Activates the immune system without pollen, and bacteria, forming tiny clumps of boogers. causing damage to the tissues Usually combined with other vaccines PARANASAL SINUSES TDAP given to children 2 months to 6 years of age Which are air-filled spaces inside the bones that surround the nose: RECAP ○ Frontal ○ Ethmoid ○ Sphenoid ○ Maxillary UPPER RESPIRATORY TRACT INFECTIONS Any infection that involves the nasal cavity, paranasal The paranasal sinuses help the inspired air to circulate sinuses, pharynx or larynx for a bit so it has time to get warm and moist ○ They also act as tiny echo chambers that help amplify the sound of your voice which is why you sound so different when they’re clogged with mucus during a cold PHARYNX (THROAT) AND LARYNX (VOICEBOX) The relatively clean, warm, and moist air goes from the nasal cavity into the pharynx or throat. At each side of the back of the throat, there is a pair of tonsils which are small clumps of lymphoid tissue that acts as body’s first line of defense that swallow viruses and bacteria that enter through the mouth or nose The lower part of the pharynx is continuous with the larynx (voicebox) It is most often caused by an invading pathogen, like a At the top of the larynx sits a spoon-shaped lap of virus. cartilage called epiglottis ○ Acts like a lid that seals the airway off when PATHWAY OF AIR IN THE UPPER RESPIRATORY you’re eating so that the food can only go one TRACT way down the esophagus and towards the stomach. NASAL CAVITY TRACHEA AND LUNGS When you breathe in, air flows through the nostrils, and enters the nasal cavity. Once the air makes its way into the larynx, it can continue ○ It is lined by cells that release mucus. to journey through the trachea or windpipe towards the lungs TRANSCRIBERS: CORPUZ, LLANTERO, LOQUIAS, PESIGAN, VERA | EDITOR: LEJANO PROOFREADER: LEJANO ACADEMICS AND RESEARCH COMMITTEE 8  TRANS 8: MICROBIAL DISEASES OF RESPIRATORY SYSTEM OTHER PARTICLES WE BREATHE (OTHER THAN TYPES OF UPPER RESPIRATORY INFECTIONS AIR) There are many different types of upper respiratory tract In addition to air, you’re constantly breathing in other stuff infections depending on the part of the tract that it’s like viruses or bacteria. involved in. ○ Example: When an infected person sneezes or coughs, they spread thousands of droplets RHINITIS containing these pathogens into the local area up to about 2 meters or 6 1⁄2 ft away. ○ These droplets can then land in the mouth or noses of people nearby or get inhaled into the upper airways Most of these viruses or bacteria can also survive on surfaces for a few hours. ○ It’s possible to get them by touching a surface like a contaminated doorknob and then touching your own eyes, nose, or mouth. PATHWAY OF PATHOGENS IN URT INFECTIONS Rhino means nose The infection is inside the nasal cavity Usually caused by viruses responsible for common cold or flu The most common is rhinovirus, influenza virus, respiratory syncytial virus (RSV), parainfluenza virus, and adenovirus When rhinitis is caused by bacteria like Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and Staphylococcus aureus ○ These bacteria often spread to the surrounding sinuses, causing rhinosinusitis Usually, even when a pathogen gets in, we’re good at ○ Rhinosinusitis - infection in both the nose and protecting ourselves, but sometimes, a particular pathogen sinuses succeeds in colonizing our upper airways and when that ○ In individuals that are immunocompromised like happens, you’ve got an infection. those taking chemotherapy, rhinosinusitis can be These infectious little pathogens typically jump inside the caused by fungi like Aspergillus. cells, lining the airways, multiply and cross over to the underlying tissue, creating an inflammatory response. PHARYNGITIS When this happens, goblet cells and submucosal glands in the airways start to produce a lot of mucus to try to trap and eventually expel these pathogens. In these severe situations, the pathogens may result in a lot of WBCs coming over to fight off these pathogens. The battle ensues with a result being passed a mixture of pathogens, immune cells, dead tissue, and a whole lot of inflammatory signaling molecules called cytokines The cytokines can then spill into the systemic circulation and reach the brain telling it to raise the body’s temperature to make it a less friendly place for those pathogens to reproduce. Infection of the pharynx or throat TRANSCRIBERS: CORPUZ, LLANTERO, LOQUIAS, PESIGAN, VERA | EDITOR: LEJANO PROOFREADER: LEJANO ACADEMICS AND RESEARCH COMMITTEE 9  TRANS 8: MICROBIAL DISEASES OF RESPIRATORY SYSTEM Can develop if a virus like rhinovirus or coronavirus decide Rhinosinusitis causes pain or pressure in the fae and to move beyond the nose and travel down into the change in voice (the tiny echo chambers get clogged up pharynx. with mucus) There are some viruses and bacteria that largely bypass Pharyngitis causes sore throat the nose and just attack the pharynx. Tonsillitis causes pain or swelling, and difficulty with ○ Example: Epstein Barr Virus or EBV swallowing Some bacteria like Group A Streptococcus can also cause Laryngitis causes horse voice and dry cough pharyngitis called strep throat. Epiglottitis causes trouble with breathing and some If the infection spread to involve the tonsils, it’s called people would describe it as a person speaking with a “hot tonsillitis potato voice” in their mouth ○ Person with epiglottitis also often is in a tripod LARYNGITIS position (leaning forward on their arms) to keep their airway open ○ A tripod position is an emergency as it is a serious infection that can block the airway DIAGNOSIS OF URT Diagnosis of an upper respiratory tract infection is usually just based on symptoms. But there are some tests that are done like rapid testing for Group A Streptococcus, EBV, and influenza. TREATMENTS OF URT Generally, for viral infections, the treatment is resolved by rest, fluids, and pain medications. Antibiotics are used for bacterial infections. Infection of the larynx SUMMARY OF URT INFECTIONS The most common is viral laryngitis caused by the usual viruses that cause the common cold and flu (Rhinovirus Upper respiratory tract infections involve the nose, and Influenza virus) sinuses, pharynx, or larynx There’s also bacterial laryngitis caused by Group A ○ They are usually caused by viruses like Streptococcus pneumoniae or Haemophilus influenzae rhinovirus but can also be due to bacteria such These bacteria, particularly Haemophilus influenzae have as Group A Streptococcus & Haemophilus special preference for the superior portion of the larynx influenzae and the epiglottis causing epiglottitis ○ Most of the time, no specific diagnostic test is However, the vaccine for Haemophilus influenzae Type B, needed and treatment is just supportive one of the more virulent subtypes of that bacteria has Except for antibiotics in the cases of made that disease much less common. bacterial infections. CLINICAL MANIFESTATIONS OF URT INFECTIONS HUMAN RHINOVIRUS (HRV) Symptoms of upper respiratory tract infections vary and A communicable infectious virus largely depend on the area involved and the cause of the Causes inflammation of the nasal mucosa (rhinitis) infection. Mainly causes URT infections Got its “rhino” name because it commonly causes a runny NON-SPECIFIC SYMPTOMS nose, nasal congestion, sneezing, sore throat, and cough There are over 100 serologic known types and all of them can cause a common cold in humans. The non-specific symptoms that can go along with many Rhinovirus belongs to the Picornaviridae family of viruses. of the infections include: ○ Fatigue ○ Loss of appetite ○ Fever SYMPTOMS OF URT INFECTIONS Rhinitis causes runny or stuffy nose and sneezing TRANSCRIBERS: CORPUZ, LLANTERO, LOQUIAS, PESIGAN, VERA | EDITOR: LEJANO PROOFREADER: LEJANO ACADEMICS AND RESEARCH COMMITTEE 10  TRANS 8: MICROBIAL DISEASES OF RESPIRATORY SYSTEM Rhinoviruses can target a few specific receptors for entry but one in particular is cellular adhesion molecule one, or ○ They are naked viruses about 30 nm in diameter ICAM-1. Naked because the capsid is not covered by a lipid membrane. ○ Surrounded by an icosahedral capsid Spherical protein shell made up of 20 equilateral triangular faces. ○ They are also single-stranded positive sense RNA viruses. This means that their RNA is actually mRNA which the host cell ribosomes use to make viral proteins. TRANSMISSION OF RHINOVIRUS Unlike other picornaviruses, rhinoviruses are Acid Labile. ○ They can be destroyed by stomach acids. This attachment allows for the rhinovirus to be eaten or ○ Hence, they don’t infect the GI tract. endocytosed into the host cell ○ They also don’t spread through fecal-to-oral routes. During the endocytosis process, the icosahedral capsid Instead, they typically infect the epithelium of the breaks open. respiratory mucosa, which lines the nasal cavity. ○ This allows the single-stranded RNA of the Transmission occurs through contact with respiratory virus to gain access to the host cell’s secretions such as snot and aerosols. cytoplasm. ○ Particularly from those who are blowing or sneezing. Touching an infected surface (e.g. door handle) followed by touching the respiratory mucosa is the main way to transfer an infection. ○ This is because rhinoviruses can survive for 2 hours on the skin and 4 hours on the surfaces. PATHWAY OF RHINOVIRUS Once the rhinovirus has been introduced to the respiratory mucosa, it targets cell surface receptors expressed at the surface of the nasal epithelial cells. In the cytoplasm, the host cell ribosomes take over viral protein production, helping the virus replicate. TRANSCRIBERS: CORPUZ, LLANTERO, LOQUIAS, PESIGAN, VERA | EDITOR: LEJANO PROOFREADER: LEJANO ACADEMICS AND RESEARCH COMMITTEE 11  TRANS 8: MICROBIAL DISEASES OF RESPIRATORY SYSTEM WHO ARE INFECTED? IMMUNOLOGIC RESPONSE OF HOST TO Rhinovirus can occur in any individual, but there are some RHINOVIRUS groups who are more susceptible: ○ Young children When the host cell realizes it has been infected, it ○ Elderly releases pro-inflammatory proteins like cytokines and ○ Immunocompromised chemokines. ○ Those with underlying respiratory diseases such as: COPD, Asthma, and Cystic fibrosis SYMPTOMS OF RHINOVIRUS The symptoms of rhinovirus are often associated with a common cold. The symptoms usually begin 1-2 days after the infection and last for about 2 weeks: ○ Nasal congestion or irritation ○ Runny nose ○ Pressure in Head, Sinus, Ear, or Face Head: which results in headache ○ Sneezing These proteins activate and attract the immune cells to the ○ Loss of smell and taste site of infection, and recruit even more immune cells from ○ Fatigue blood vessels in the lamina propria, the layer just under ○ Malaise the epithelium in the respiratory mucosa. ○ Loss of appetite ○ Sore throat, a cough, or hoarseness While symptoms are usually mild, factors such as the following can result in much more drastic manifestations, and sometimes even more complicated and life-threatening symptoms: ○ Age ○ Immunocompromised state ○ Underlying respiratory diseases DIAGNOSIS OF RHINOVIRUS Rhinovirus is mainly diagnosed clinically specially when The end result is local inflammation common cold symptoms are present without additional complications, concerning physical finding, and relevant history. Definitive diagnosis can be made with PCR testing from secretions or washings ○ BUT this is typically only done in complex cases such as those who are immunocompromised or have underlying respiratory disease. TRANSCRIBERS: CORPUZ, LLANTERO, LOQUIAS, PESIGAN, VERA | EDITOR: LEJANO PROOFREADER: LEJANO ACADEMICS AND RESEARCH COMMITTEE 12  TRANS 8: MICROBIAL DISEASES OF RESPIRATORY SYSTEM TREATMENTS OF RHINOVIRUS Because rhinovirus tend to be mild and self-limited, the treatments focus on relieving symptoms and preventing other people from becoming infected: ○ Rest ○ Hydration ○ Age-appropriate over the counter (OTC) medications: First generation antihistamines NSAIDs (Non-steroidal anti-inflammatory drugs) Nasal decongestants General precautions are also followed to limit the spread of the virus such as: ○ Covering coughs and sneezes ○ Washing hands (especially after nose blowing) ○ Regular disinfection of surfaces SUMMARY OF RHINOVIRUS Rhinovirus is a type of Picornavirus which is the common cause of common cold. It infects the epithelium of the respiratory mucosa through a nasal route of transmission A consequence of the inflammatory response from the immune cells leads to rhinitis The hallmark symptoms of common cold include: runny nose, nasal congestion, and sneezing. A clinical diagnosis is usually made and treatment tends to center on symptom relief and preventing the spread of infection to others. PNEUMONIA Infection of the lower respiratory tract airways and lung parenchyma The cause varies by age ○ 2 most common causes: Bacterial and Viral May be a complication of systemic viral illness like measles or chickenpox Single largest contributor of childhood mortality worldwide TRANSCRIBERS: CORPUZ, LLANTERO, LOQUIAS, PESIGAN, VERA | EDITOR: LEJANO PROOFREADER: LEJANO ACADEMICS AND RESEARCH COMMITTEE 13  TRANS 8: MICROBIAL DISEASES OF RESPIRATORY SYSTEM PNEUMONIA CATEGORIES STAGES SYMPTOMS Dyspnea Chest pain Productive cough – pus or bloody sputum Systemic symptoms ○ Fatigue ○ Fever DIAGNOSIS working hard to breathe breathing quickly chest x-ray dullness to percussion ○ lung consolidation tactile vocal fremitus ○ more vibrations from person's back on repeating certain phrases late inspiratory crackles bronchial breath sounds Bronchophony Egophony TREATMENT Depends on severity Antibiotics Cough suppressants Pain Medications MYCOPLASMA PNEUMONIAE Atypical Pneumonia in young adults Cell membrane ○ Sterol ○ Lack rigid cell wall ○ Don’t take up dye under gram staining ○ Can’t be visualized with light microscopy Highly Pleomorphic Osmotically unstable in external environment Invades host cells and live intracellularly Facultative anaerobe TRANSCRIBERS: CORPUZ, LLANTERO, LOQUIAS, PESIGAN, VERA | EDITOR: LEJANO PROOFREADER: LEJANO ACADEMICS AND RESEARCH COMMITTEE 14  TRANS 8: MICROBIAL DISEASES OF RESPIRATORY SYSTEM ○ Grows better in an aerobic environment Prefers the lungs and respiratory airways Transmission: respiratory droplets through sneezing and coughing Occurs mostly in: ○ Children at school ○ Young adults in college ○ Military recruits PATHWAY OF PATHOGENS IN MYCOPLASMA PNEUMONIA Sputum sample ○ Looks like fried eggs SYMPTOMS Asymptomatic Nonspecific symptoms ○ Fatigue ○ Sore throat Cold agglutinin ○ Mild fever ○ Dry Hacking cough Other bacterial Pneumonia ○ Dyspnea ○ Fever ○ Chest pain ○ Productive cough Encephalitis ○ In children Fever Changes in mental status Neck stiffness DIAGNOSIS When Encephalitis is suspected Lumbar puncture is done Chest x-ray ○ CSF Analysis TREATMENT Generally Self-Limiting Antibiotics ○ Cell wall inhibitors are inefficient ○ Thus, treatment relies on antibiotics that inhibit protein biosynthesis Tetracyclines ○ Macrolides Erythromycin Azithromycin TRANSCRIBERS: CORPUZ, LLANTERO, LOQUIAS, PESIGAN, VERA | EDITOR: LEJANO PROOFREADER: LEJANO ACADEMICS AND RESEARCH COMMITTEE 15  TRANS 8: MICROBIAL DISEASES OF RESPIRATORY SYSTEM PERTUSSIS Nasal congestion Cough Contagious infection caused by the bacteria Bordetella Low-grade fever Pertussis ○ Very contagious Causes violent coughing spells called paroxysms making 3. Paroxysmal Phase (1-6 weeks) it difficult to breathe ○ Symptoms persist from damage by bacteria, Causes partially swollen airways which makes a whooping most notable: noise Paroxysms like a “Machine gun bursts” A.K.A “Whooping Cough” Uninterrupted fit of coughing Whooping noise TRANSMISSION These symptoms can cause: Vomiting Sneeze or cough when droplets land in mouth, nose, or is Collapsed lung inhaled at about 2 meters or 6 feet away Broken rib Contaminated surfaces (e.g. doorknobs) as it can also Petechiae survive for several days on dry surfaces, ○ Infant symptoms: Gasping MECHANISM Cyanosis Apnea Apparent Life Threatening Event (ALTE) BORDETELLA PERTUSSIS Decreased O2 Levels 4. Convalescent Phase (2-3 weeks) Gram Negative coccobacilli (short pink rod) ○ Cough slowly improves Releases toxins that help the bacteria attach or anchor to ○ Paroxysms and whooping fade epithelium ○ Airway heals ○ Filamentous Hemaglutinin ○ Pertactin DIAGNOSIS ○ Agglutinin ○ Tracheal cytotoxin Best to diagnose Pertussis during the Catarrhal phase Paralyzes the cilia so it can’t be swifted ○ Because antibiotics can kill bacteria to reduce back damage ○ Pertussis toxin Methods: Causes an increase in T-cell population 1. Growing the bacteria in a culture Blocks T-cells from migrating into Identifying DNA of bacteria by infected tissues Polymerase Chain Reaction Makes the blood vessels in the 2. Direct fluorescent antibody respiratory tissue more sensitive to Detects Bordetella Pertussis antigens histamine, making it easier for fluid to 3. Pertussis serology seep out of the blood vessels and into Looking for antibody response to the airway tissues–causing the classic pertussis (detectable after the infection whooping cough has gone on for a few weeks ○ Adenylate cyclase Infants - Degree of lymphocytosis Blocks the phagocyte from getting into the site of infection Induces phagocytes to undergo TREATMENT apoptosis Marclide antibiotics - Azithromycin Mucous starts building up, triggering a violent cough reflex ○ Used when bacteria are still alive in the Catarrhal to clear the airway or early Paroxysmal phase Prevent transmission to infants and immunocompromised PERTUSSIS INFECTION ○ Isolate infected person ○ Antibiotic prophylactics to household contacts 1. Incubation Period (1 week) ○ Infants monitored closely ○ Time between the bacteria entering the body and ○ Pregnant women - vaccine in 3rd trimester to the onset of symptoms generate antibodies, offering passive immunity to ○ Bordetella Pertussis is already in the respiratory the baby tract but has not multiplied enough 2. Catarrhal Phase (2 weeks) PERTUSSIS VACCINE ○ Bacterial concentration increases, causing damage in the respiratory tract causing Avoid the disease or lessen symptoms symptoms like: DTAP TRANSCRIBERS: CORPUZ, LLANTERO, LOQUIAS, PESIGAN, VERA | EDITOR: LEJANO PROOFREADER: LEJANO ACADEMICS AND RESEARCH COMMITTEE 16  TRANS 8: MICROBIAL DISEASES OF RESPIRATORY SYSTEM ○ Diphtheria, Tetanus, and Acellular Pertussis ○ Has a thin peptidogylcan layer ○ 90% effective ○ Doesn’t retain violet dye during gram staining Outbreaks: ○ Stains pink with the safranin dye ○ Countries that do not have access to the vaccine Non-motile and facultative anaerobic ○ Communities with high rate of unvaccinated Catalse and oxidase positive individuals ○ Among the elderly (low leverls of antibody) CULTIVATION COMMUNITY ACQUIRED PNEUMONIA Chocolate agar - as it contains nutrients that Haemophilus needs to grow Caused by the bacteria Haemophilus Influenzae ○ Factor X (Hemin) ○ Gram-negative coccobacillus ○ Factor V (Nicotinamide Adenine Nucleotide) ○ Two major categories: Blood agar with Staphylococcus Aureus Encapsulated ○ Factor V via RBCs hemolysis Classified into 6 serotypes: A, Properties: B, C, E, and F ○ Convex, smooth, gray or transparent colonies Unecapsulated Nontypable - because they lack the polysaccharide capsule ENCAPSULATED HAEMOPHILUS INFLUENZAE consequently capsular Specific Parts antigens ○ Polysaccharide (Capsule) Major virulence factor because of its TRANSMISSION antiphagocytic ability ○ Pili Hair like extensions that have adhesion Respiratory droplets and secretions proteins (HMW1 and HMW2) which help attach to host cells H. INFLUENZAE TYPE B ○ Phase variation Can change the oligosaccharides that it Risk Factors: expresses on its outer membrane each ○ Children time they infect a cell ○ Spleen issues Immune system cannot remember the Splenectomy infective strain, so it is unable to Sickle Cell Disease produce a quick specific immune ○ Malignancies response ○ Congenital deficiency of complement ○ Biofilms components Exopolysaccharides (EPS) ○ Acute viral infection Causes more invasive disease ○ Epiglottitis - Nasopharynx to the epiglottis H. INFLUENZAE NONTYPABLE ○ Cellulitis - Nasopharynx to soft skin tissues in the face Risk Factors: ○ Bactermia - Nasopharynx to blood capilliaries ○ Children Meninges -> Meningitis ○ Immunocompromising conditions Bones -> Osteomyelitis Diabetes Joints -> Septic Athritis Malignancy Colonizes 3-5% of children aged 2-5 years HIV infection Viral infections NONENCAPSULATED HAEMOPHILUS INFLUENZAE Postviral pneumonia Underlying lung condition Causes less invasive disease - mostly only cause mucosal COPD (bronchopneumonia) infections by direct extension Cystic fibrosis ○ Middle ear -> Otitis media ○ Parasnasal sinuses -> Sinusitis MECHANISM ○ Bronchi -> Bronchitis ○ Lungs -> Pneumonia HAEMOPHILUS INFLUENZAE Colonizes 40-80% of children and adults Strain that cause disease in human ○ Type B or HIB BOTH ENCAPSULATED AND UNCAPSULATED ○ Nontypable Gram negative Outer membrane (Lipooligosaccharides or LOS) TRANSCRIBERS: CORPUZ, LLANTERO, LOQUIAS, PESIGAN, VERA | EDITOR: LEJANO PROOFREADER: LEJANO ACADEMICS AND RESEARCH COMMITTEE 17  TRANS 8: MICROBIAL DISEASES OF RESPIRATORY SYSTEM ○ Inhibits mucociliary clearance or self-cleaing ○ Bronchoalveolar lavage mechanism of bronchi Serological Methods: Produces IgA protease ○ Latex agglutination ○ Destroys immunoglobulin A (IgA) ○ Enzyme immunoassay Normally opsonizes invading bacteria ○ Coagglutination Epiglotittis SYMPTOMS ○ Laryngoscopy - shows a cherry red swollen epiglottis H. INFLUENZAE TYPE B ○ X-ray - shows a thumbprint sign Bronchopneumonia ○ Chest x-ray - show ground-glass opacities, bronchial wall thickening, and confluent areas of consolidation TREATMENT Vaccine ○ 2-18 months of age ○ Contains Type B capsular polysaccharide conjugated to the diphtheria toxoid component H. INFLUENZAE TYPE B Meningitis ○ Ceftriaxone ○ Chloramphenicol Children ○ Chemoprophylaxis by using Rifampin H. INFLUENZAE NONTYPABLE Mucosal infections ○ First-line: Amoxicillin with or without Clavulanate ○ Alternatives: 3rd and 2nd Gen Cephalosporins, Macrolides, and Fluoroquinolones LEGIONELLA PNEUMOPHILA H. INFLUENZAE NONTYPABLE A gram-negative bacillus which means is shaped like a rod and can be found in many water systems such as: ○ hot water tanks ○ cooling towers ○ large air conditioning systems ○ hot tubs Is typically transmitted by inhaling infected aerosols like contaminated water sprays, jets, or mists DIAGNOSIS Biological Sample: ○ Blood ○ CSF ○ Synovial Fluid ○ Pleural Fluid ○ Fluid from sinus aspiration ○ Tympanocentesis ○ Trachehal or lung aspiration ○ Bronchoscopy TRANSCRIBERS: CORPUZ, LLANTERO, LOQUIAS, PESIGAN, VERA | EDITOR: LEJANO PROOFREADER: LEJANO ACADEMICS AND RESEARCH COMMITTEE 18  TRANS 8: MICROBIAL DISEASES OF RESPIRATORY SYSTEM Causes a disease called Legionellosis with two distinct OXIDASE & CATALASE POSITIVE entities. It produces both these enzymes. LEGIONELLOSIS GROW ON BUFFERED CHARCOAL YEAST EXTRACT LEGIONNAIRES’ PONTIAC FEVER (BCYE) DISEASE It needs special nutrients to grow such as cysteine and A deadly outbreak of Got its name from Pontiac, iron so it grows on a special medium called Buffered pneumonia in 1976 among Michigan, where the first Charcoal Yeast Extract which contains cysteine and iron people attending a case was recognized. that are essential for growth of Legionella. convention of the American ○ In this medium, it forms gray-white colonies with Legion. a cut glass appearance. A much milder disease without pneumonia, but with Causes a severe some flu-like symptoms. pneumonia with high fevers, usually over 40 degrees celsius or 104 degrees Fahrenheit. TRANSMISSION There can also be gastrointestinal Can enter the body through inhalation of contaminated symptoms, such water droplets. as: ○ vomiting ○ diarrhea Neurological symptoms such as: ○ headache ○ confusion THIN PEPTIDOGLYCAN Has a very thin peptidoglycan layer so it stains like a Once it reaches the lungs, it gets ingested by alveolar gram-negative bacteria. macrophages and inside macrophages, it gets wrapped But it stains pretty weakly as a gram-negative bacteria, up in a vesicle called phagosome which normally merges so it's best visualized with silver stain. with lysosomes to kill invading bacteria. However, Legionella has a type 4b secretion system NON-SPORE FORMING AEROBIC which uses effector proteins to prevent phagolysosomal fusion. It needs oxygen to survive. ○ As a result, Legionella is able to survive and replicate inside macrophages. FACULTATIVE INTRACELLULAR It can survive both inside and outside the cell TRANSCRIBERS: CORPUZ, LLANTERO, LOQUIAS, PESIGAN, VERA | EDITOR: LEJANO PROOFREADER: LEJANO ACADEMICS AND RESEARCH COMMITTEE 19  TRANS 8: MICROBIAL DISEASES OF RESPIRATORY SYSTEM Dissemination of bacteria to other sites outside the lungs, such as: central nervous system, GI tract, kidneys, and heart may occur via infected macrophages that carry the bacteria. DIAGNOSIS Cultures from respiratory tract secretions Urinary Antigen Test that detects Legionella lipopolysaccharide antigen in urine. Chest x-ray that shows Apache infiltrate with consolidation of one lobe Blood analysis shows: ○ Hyponatremia - low levels of sodium in the blood ○ Leukocytosis - high levels of leukocytes When the cells become too small for the growing number ○ Thrombocytopenia - low levels of thrombocytes. of bacteria, it bursts, releasing Legionella in the extracellular space and infecting other cells. Bacterial growth and death of alveolar macrophages produce powerful chemotactic factors that cause a large influx of polymorphonuclear leukocytes and monocytes from the peripheral blood. TREATMENT LEGIONNAIRES’ DISEASE PONTIAC FEVER Macrolides Pontiac fever is a azithromycin self-limiting disease that Fluoroquinolones resolves spontaneously and levofloxacin does not require treatment RECAP Legionella Pneumophila is a gram-negative bacillus found in water systems. This leads to fluid exudation and deposition of fibrin in It is a non-spore forming, aerobic, facultative intracellular, the aalveoli, resulting in a destructive pneumonia that catalase and oxidase-positive bacteria that is best obliterates the air spaces and compromises respiratory visualized with silver stain function. Grows well on BCYE agar with cysteine and iron into