Week 10 Infectious Disease Notes PDF

Infectious Disease 13: Upper Respiratory Infections (URIs) 1. Outline the main pathogens that cause different types of URIs 2. Discuss the main clinical manifestations of URIs 3. Discuss the diagnostic approach to differ...

Infectious Disease 13: Upper Respiratory Infections (URIs) 1. Outline the main pathogens that cause different types of URIs 2. Discuss the main clinical manifestations of URIs 3. Discuss the diagnostic approach to different types of URIs URI Areas Main pathogens Clinical manifestations Diagnosis Treatment Ottis Media Virus or Most in children tympanocentesis Amoxicillin (Middle ear) bacteria=Streptococcus Otalgia (ear pain) pneumoniae is the most tympanic common cause. membrane is Haemophilus influenzae erythematous and Moraxella catarrhalis are also common causes. Among viruses, respiratory syncytial virus, coronaviruses (common cold strains), and rhinoviruses are commonly involved Sinusitis S. pneumoniae, H. nasal discharge, Arrow points to Amoxicillin influenzae, and M. nasal congestion, opacified maxillary catarrhalis, as in the facial or sinus pain sinus seen in case of acute otitis decreased sense of computed tomography media.In smell, and fever. scan of head immunocompromised Headache and patients and diabetics, malodorous breath sinusitis caused by fungi such as Aspergillusor Mucor may occur. Pharyngitis S. pyogenes (GAS) Gray exudate on A throat culture is penicillin G, penicillin V, Neisseria inflamed tonsils the most reliable or amoxicillin gonorrhoeae is likely Petechiae on the method of If allergic- erythromycin to be the result of palate is a determining or cephalexin sexual activity diagnostic clue for whether S. Mycoplasma GAS pharyngitis pyogenes is the pneumoniae, cause. Chlamydia Pharyngitis caused pneumoniae, and by Epstein–Barr Arcanobacterium virus. Note several haemolyticum whitish exudates on Viruses- adenovirus, tonsils (red arrow). influenza A and B viruses, parainfluenza virus, rhinovirus Common Cold Rhinoviruses (more than nasal congestion, Erythematous and Zinc Salt 100 serotypes) are the decreased sense of edematous nasal most common etiology smell, rhinorrhea mucosa is seen on (up to 50%). (watery nasal physical examination. Coronaviruses, discharge without Conjunctival and adenoviruses, and purulence), and pharyngeal injection enteroviruses such as sneezing may also be seen. Coxsackie viruses. Coup- larynx, Parainfluenza viruses, barking cough and a Plain radiographs may Dexamethasone, w/ or trachea, and especially type 1, are hoarse voice show a “steeple sign” without epinephrine large bronchi the most common cause (subglottic tracheal (laryngotracheo narrowing results in an bronchitis) inverted “V” shape) Laryngitis Parainfluenza viruses inability to speak Hydration and voice rest and rhinoviruses are the (aphonia) most common causes of laryngitis Epiglottitis H. influenzae type B is, odynophagia (pain on “cherry-red” epiglottis Ceftraxone by far, the most common swallowing) or may be visualized. On dysphagia (difficulty in lateral plain X-rays, an swallowing) enlarged epiglottis may be seen as a “thumb” sign Infectious Disease 14: Lower Respiratory Infections 1. Outline the main pathogens that cause different types of LRIs 2. Discuss the main clinical manifestations of different types of LRIs 3. Understand the pathophysiology behind pleural effusions A pleural effusion occurs when excess fluid accumulates in the pleural space—the area between the chest cavity and the lungs—restricting lung expansion. The pleural space is bordered by the parietal pleura, attached to the chest wall, and the visceral pleura, attached to the lungs. Normally, this space contains a thin layer of fluid, similar to interstitial fluid, which allows the lungs to move smoothly during breathing. Fluid in the pleural space originates from plasma that leaks from nearby capillaries. Under normal circumstances, lymphatic vessels in the pleura drain this fluid. An effusion arises when there is either excessive fluid production or impaired drainage. Types of Pleural Effusion 1. Transudative Effusion: ○ Caused by changes in hydrostatic or oncotic pressure in the blood vessels. ○ Hydrostatic pressure: Increased pressure (e.g., due to heart failure) forces fluid out of capillaries.  ○ Oncotic pressure: Decreased pressure (e.g., from cirrhosis or nephrotic syndrome) allows fluid to leak into the pleural space. 2. Exudative Effusion: ○ Results from inflammation that increases capillary permeability, allowing fluid, immune cells, and proteins to leak. ○ Causes include infections (like pneumonia), trauma, malignancy, or inflammatory diseases. 3. Lymphatic Effusion (Chylothorax): ○ Occurs when the thoracic duct is disrupted, leading to lymph fluid accumulation. This is often due to surgical damage or tumors compressing the duct. Symptoms and Diagnosis Symptoms of pleural effusion depend on the size of the effusion: Small effusions may be asymptomatic. Larger effusions can cause pleuritic pain, shortness of breath, and symptoms may worsen when lying flat. Physical examination findings include: Decreased breath sounds Dullness to percussion Decreased tactile fremitus (reduced vibrations felt on the chest wall when speaking). Imaging, particularly X-rays, can reveal fluid accumulation, especially at the costophrenic angle or along the chest wall when lying down. Treatment Diagnosis typically involves thoracentesis, a procedure to drain fluid and alleviate symptoms. The fluid is analyzed to distinguish between transudative and exudative effusions using Light's Criteria, which assesses protein and LDH levels. 4. Understand the differences in the types of fluid that can accumulate in the pleural space High leukocytosis Criteria for Transudate (Light’s Criteria): Pleural protein/serum protein < 0.5 Pleural LDH/serum LDH < 0.6 Pleural LDH < 2/3 of the upper limit of normal for serum LDH. Criteria for Exudate (Light’s Criteria): Pleural protein/serum protein > 0.5 Pleural LDH/serum LDH > 0.6 Pleural LDH > 2/3 of the upper limit of normal for serum LDH. Area/Disease Pathogens/ Clinical Diagnosis Treatment Pathophysiology manifestations Bronchitis - cough due to virus. Cough Chest radiograph oseltamivir (Tamiflu) Smoking damage cilia= no hyperactivity, nasal clearing mucous congestions - Respiratory viruses (influenza A and B, parainfluenza virus, coronavirus, rhinovirus, respiratory syncytial virus [RSV], and human metapneumovirus) Bronchiolitis RSV -under 2 years old Enzyme Ribavirin -hypoxia, apnea, immunoassay (EIA) and respiratory for RSV antigen failure Pneumonia -Drugs and age are Rusty Sputum macrolide such as predisposing factors azithromycin, a -S. pneumoniae H. tetracycline such as influenzae. doxycycline, or a Staphylococcus aureus respiratory quinolone Mycoplasma pneumoniae, such as levofloxacin Legionella species Lung Abscess -aspirate oropharyngeal -fatigue, night Clindamyosin bacteria into the lower sweats airways and alveoli -sputum is foul, full -Peptostreptococcus of anaerobes species, Prevotella -cough, fever species, and Fusobacterium nucleatum -air-fluid Lung Apnea -collection of pus in pleural -fever, cough chest Ultrasound and CT Surgical drainage  space=many neutrophils pain to find localization -S. pneumoniae is the -cannot be resolve most common cause of with antibiotics empyema; however, members of the Streptococcus anginosus group are often found. Infectious Disease 15: Mycobacteria and other Acid-Fast Bacteria 1. Discuss the microscopic and growth characteristics of Mycobacteria and other Acid-Fast Bacteria ○ Acid-fast bacteria are a group of bacteria that have a unique cell wall structure that makes them resistant to certain types of staining and decolorization. ○ Mycobacteria are slender bacilli (rods) with lipid-rich cell walls that are resistant to penetration by chemical dyes such as those used in the Gram stain. ○ unique class of very long–chain (75-90 carbons), β-hydroxylated fatty acids (mycolic acids)- waxy cell surface that makes mycobacteria strongly hydrophobic and accounts for their acid-fast staining characteristic  2. Outline the host risk factors, mode of transmission, and pathophysiology of diseases caused by Mycobacteria and other Acid-Fast Bacteria ○ This organism is a cause for special concern in immunocompromised patients, particularly those infected with HIV.- nearly 50% of the HIV-infected population is coinfected with M. tuberculosis. bacterial sulfolipids inhibit the fusion of phagocytic vesicles with lysosomes ○ transmission is person to person by inhalation of the aerosol ○ antibodies appear, they do not contribute to clearance of the organism. Instead, cellular immunity (CD4+ T cells) and the accompanying delayed hypersensitivity ★ In summary, immunity to M. tuberculosis is primarily mediated by Th1 cells, which stimulate macrophages to kill the bacteria. This immune response, although largely effective, comes at the cost of accompanying tissue destruction. ★ Lysing of erythrocyte (low hemoglobin) - use cold titer 3. Discuss the clinical manifestations and most common complications of diseases caused by Mycobacteria and other Acid-Fast Bacteria the initial pulmonary nodule (a healing tubercle; see above) and some fibrosis ○ Initial phase- engulf of phagocytes and inflammatory reaction in the alveolus Asymptomatic until one month ○ Tubercule formation- granuloma or a tubercle that consists of a central area of large, multinucleated giant cells (macrophage syncytia) containing tubercle  bacilli, a midzone of pale epithelioid cells, and a peripheral collar of fibroblasts and mononuclear cells. Tissue damage is produced by the destruction of both bacilli and phagocytes, which results in the release of degradative enzymes and reactive oxygen species such as superoxide radicals= (cheesy) necrosis ○ Course- cavity is created that can facilitate spread of the infection ○ Secondary- reactivation= “caseous necrosis”- Destruction of the lung tissue leads to air-filled cavities where the bacteria replicate actively. Bacterial populations in such lesions often become quite large, and many organisms are shed (eg, in sputum). The patient becomes capable of exposing others to the disease. Miliary pulmonary disease occurs when organisms draining through lymphatics enter the venous blood and circulate back to the lung. Systematic- happens to spleen which in pic above.  (D) In this specimen from an immunocompromised patient, macrophages with large numbers of mycobacteria are seen (acid-fast stain). 4. Discuss the diagnostic approach to diseases caused by Mycobacteria and other Acid-Fast Bacteria ○ TB test- Mantoux test, purified protein derivative (PPD) is prepared from culture filtrates of the organism and biologically standardized. Activity is expressed in tuberculin unit ○ Lab- Lowenstein-Jensen medium.  ○ Nuclear amplification- PCR ○ Treatment- Isoniazid, rifampin, ethambutol, streptomycin, and pyrazinamide are the principal or “first-line” drugs Other Bacteria Acid-Fast: Name Growth/Microscopic Clinical Treatment characteristics Manifestations/ Diagnosis Mycobacterium contact with or ingestion -Leprosy is a chronic -dapsone, rifampin, and of armadillos granulomatous clofazimine leprae condition of -Thalidomide, an inhibitor of tumor peripheral nerves and necrosis factor-α, is being mucocutaneous distributed under tight restrictions tissues, particularly for use as a treatment for erythema the nasal mucosa nodosum leprosum, a serious and severe skin complication of leprosy. Actinomycetes -group of filamentous, - presence of “sulfur -Penicillin G branching, gram-positive granules” in the organisms that easily draining fragment into slender pus=yellowish rods particles, which, in -part of the normal oral fact, do not contain and intestinal flora in sulfur humans. The organism is -thioglycollate broth a strict anaerobe or blood agar -​​aerobic soil organisms -presentation of -Trimethoprim-sulfamethoxazole Nocardia -inhaled or acquired by human (TMP-SMX) contamination of skin nocardiosis is a asteroides and wounds pneumonia of rather chronic Nocardia course with brasiliensis abscesses, extensive necrosis, and cavity formation Atypical -Group I contains the - chronic pulmonary photochromogens, which disease Mycobacteria- produce pigment in the -cervical adenitis in Mycobacterium kansasii light children and is found in raw milk, and Mycobacterium dairy products, soil, marinum. M. kansasii and water Infectious Disease 16: Mycoplasmas and Chlamydiae 1. Discuss the microscopic and growth characteristics of Mycoplasmas and Chlamydiae 2. Outline the host risk factors, mode of transmission, and pathophysiology of diseases caused by Mycoplasmas and Chlamydiae  3. Discuss the clinical manifestations and most common complications of diseases caused by Mycoplasmas and Chlamydiae 4. Discuss the diagnostic approach to diseases caused by Mycoplasmas and Chlamydiae Bacteria Name Microscopic/ Mode of transmission/ Clinical Manifestations/ Treatment growth Pathophysiology Diagnosis characteristics Mycoplasmas -lack cell wall -exposure to the -wheezing, asthma, macrolide, -require sterols for respiratory secretions and other reactive tetracycline, or growth of persons harboring airway diseases quinolone -“fried egg” the organism -limited to the appearance -Specialized adhesin respiratory tract and adherence -sore scratchy throat accessory proteins are and persistent cough part of this tip-mediated -tracheobronchitis and attachment organelle bronchopneumonia that helps the -brain- encephalitis organisms bind to -PCR assay carbohydrate-containin g receptors on the respiratory epithelium. -community-acquired respiratory distress  syndrome (CARDS) toxin exhibits similarities to pertussis toxin= hyperinflammation. Chlamydiae -Gram-negative -C trachomatis is the adults-In female, cervix Doxycycline (not bacteria that have leading bacterial agent (cervicitis) to the children or an obligatory of sexually transmitted endometrium pregnant) and requirement to grow disease (STD) (endometritis), then to azithromycin or and propagate -Lymphogranuloma the fallopian tubes clarithromycin (if within eukaryotic cells venereum (LGV, (salpingitis). In men persisted) -cannot be serovars L1-L3)- with urethritis, the cultured in nutrient causes an invasive organisms can broth media or on disease primarily of the eventually colonize the agar plates lymph nodes epididymis -“stealth -Trachoma (epididymitis) and the pathogens”= higher -direct contact with prostate (prostatitis) evasion of host mucous membranes or but rarely the testicles immune abraded skin, that is, (orchitis). - outer membrane by sexual contact containing -Infants- may develop lipopolysaccharide (truncated and not conjunctivitis and very endotoxic) and pneumonia that is a cytoplasmic characterized by a membrane chronic, repetitive -function in taking cough without ATP from the host wheezing to ensure sufficient quantities to drive -NAATs, such as PCR, their synthetic and - the infectious ligase chain reaction, metabolic needs. or extracellular form called an elementary transcription-mediated body (EB)-attach- and amplification the noninfectious but metabolically active intracellular form called a reticulate body (RB) -EBs then transform  into RBs, the chromosome becomes relaxed and transcriptionally active, and metabolic growth and binary fission ensue to generate progeny. Convert back to EB to leave. Infectious Disease 17: Haemophilus and Related Bacteria 1. Discuss the microscopic and growth characteristics of Haemophilus spp and related bacteria ○ cell wall- lipopolysaccharide with endotoxin activity is present in the cell wall ○ covered with a polysaccharide capsule,and six antigenic serotypes ( a through f ) have been identified. Before the introduction of the H. influenzae type b vaccine, H. influenzae serotype b was responsible for more than 95% of all invasive Haemophilus infections.  ○ eight biotypes (I through VIII) as determined by three biochemical reactions: indole production, urease activity, and ornithine decarboxylase activity. 2. Identify the growth requirements for Haemophilus spp and related bacteria ○ growth-stimulating factors: (1) hemin (also called X factor for “unknown factor”) and (2) nicotinamide adenine dinucleotide ( NAD; also called V factor for “vitamin”). ○ 3. Outline the risk factors, mode of transmission, and pathophysiology of diseases caused by Haemophilus spp and related bacteria ○ common cause of disease in unvaccinated children (i.e., meningitis, epiglottitis [obstructive laryngitis], cellulitis) ○ Cell wall components of the bacteria (e.g., lipopolysaccharide and a low-molecular-weight glycopeptide) impair ciliary function, leading to damage of the respiratory epithelium. ○ The major virulence factor in H. influenzae type b is the antiphagocytic polysaccharide capsule, which contains ribose, ribitol, and phosphate (commonly referred to as polyribitol phosphate [PRP] ). ○ (Ig)A1 proteases 4. Understand the virulence factors of Haemophilus spp and related bacteria ○ Question 3 5. Discuss the clinical manifestations of diseases caused by Haemophilus spp and related bacteria ○ Meningitis- bacteremic spread of the organisms from the nasopharynx ○ Epiglottis- cellulitis and the swelling of the supraglottic tissues, represents a life-threatening emergency ○ Arthritis- most common form of arthritis in children younger than 2 years was an infection of a single, large joint secondary to bacteremic spread of H. influenzae type b. ○ Cellulitis- development of reddish-blue patches on the cheeks or periorbital areas. ○ Otitis, Sinusitis, and Lower Respiratory Tract Disease- H. influenzae and Streptococcus pneumoniae are the two most common causes of acute and chronic otitis and sinusitis. commonly colonize patients who have chronic pulmonary disease (including cystic fibrosis), and are frequently associated with exacerbation of bronchitis and frank pneumonia ○ Conjunctivitis- H. aegyptius, also called the Koch-Weeks bacillus, causes an acute purulent conjunctivitis ○ Chancroid- caused by H. ducreyi, is a sexually transmitted disease that is most commonly diagnosed in men, presumably because women can have asymptomatic or inapparent disease. Lesion ulcerates and becomes painful, and inguinal lymphadenopathy is commonly present. ○ Both blood and cerebrospinal fluid (CSF) should be collected from patients with the diagnosis of meningitis. ○ Antigen detection= PRP capsular antigen ○ Satellite phenomenon= Staphylococcus aureus excretes nicotinamide adenine dinucleotide (NAD, or V factor) into the medium, providing a growth factor required for Haemophilus influenzae (small colonies surrounding S. aureus colonies [arrow]). ○ Treatment- Serious infections are treated with broad-spectrum cephalosporins. Less severe infections, such as sinusitis and otitis, can be treated with amoxicillin (if susceptible; approximately 30% of strains  are resistant), an active cephalosporin, azithromycin, doxycycline, or a fluoroquinolone. Others: Aggregatibacter- species colonize the human mouth and can spread from the mouth into the blood and then stick to a previously damaged heart valve or artificial valve, leading to the development of endocarditis Pasteurella- small, facultatively anaerobic, fermentative coccobacilli, commonly found as commensals in the oropharynx of healthy animals. Grows well on blood and chocolate agars. (1) localized cellulitis and lymphadenitis that occur after an animal bite or scratch ( P. multocida from contact with cats or dogs; P. canis from dogs); (2) an exacerbation of chronic respiratory disease in patients with underlying pulmonary dysfunction (presumably related to colonization of the patient’s oropharynx followed by the aspiration of oral secretions); and (3) a systemic infection in immunocompromised patients, particularly with hepatic disease. Production of a polysaccharide capsule composed of hyaluronic acid is an important virulence factor in Pasteurella strains responsible for animal diseases and is likely to be important in human infections Infectious Disease 20: The Enterobacteriaceae 1. Discuss the microbiology characteristics of enterobacteriacea ○ Ubiquitous (found everywhere) organisms found worldwide in soil, water, and vegetation and are part of the normal intestinal flora of most animals, including humans. ○ non–spore-forming, gram-negative rods that share a common antigen (enterobacterial common antigen). All members can grow rapidly, aerobically and anaerobically (facultative anaerobes), on a variety of nonselective (e.g., blood agar) and selective (e.g., MacConkey agar) media. ○ The absence of cytochrome oxidase activity is an important characteristic, because it can be measured rapidly with a simple test and is used to distinguish the Enterobacteriaceae from many other Bipolar staining ○ heat-stable lipopolysaccharide (LPS) is the major cell wall antigen and consists of three components: the outermost somatic O polysaccharide, a core polysaccharide common to all Enterobacteriaceae (enterobacterial common antigen mentioned earlier), and lipid A ○ The epidemiologic (serologic) classification of the Enterobacteriaceae is based on three major groups of antigens: somatic O polysaccharides, K antigens in the capsule (type-specific polysaccharides), and H proteins in the bacterial flagella.  2. Discuss the pathophysiology and immunity against enterobacteriacea ○ Endotoxin is a virulence factor shared among aerobic and some anaerobic gram-negative bacteria. The activity of this toxin depends on the lipid A component of LPS, which is released at cell lysis. ○ Encapsulated Enterobacteriaceae are protected from phagocytosis by the hydrophilic capsular antigens, which repel the hydrophobic phagocytic cell surface. ○ expression of the somatic O antigens, capsular K antigens, and flagellar H antigens is under the genetic control of the organism- protects the bacteria from antibody-mediated cell death ○ type III secretion system as a molecular syringe consisting of approximately 20 proteins that facilitate transfer of bacterial virulence factors into the targeted host cells ○ Iron is an important growth factor required by bacteria, but it is bound in heme proteins (e.g., hemoglobin, myoglobin) or in iron-chelating proteins (e.g., transferrin, lactoferrin). The bacteria counteract the binding by producing their own competitive siderophores or iron-chelating compounds ○ E. coli- heat-stable toxins (STa and STb) and heat-labile toxins (LT-I, LT-II). High Sta will increase cGMP while LT1 increase cAMP One protein, translocated intimin receptor (Tir), is inserted into the epithelial cell membrane and functions as a receptor for an outer membrane bacterial adhesin, intimin. Binding of intimin to Tir results in polymerization of actin, accumulation of cytoskeletal elements beneath the attached bacteria, loss of cell-surface integrity, and eventual cell death. hemolysin HlyA, which lyses erythrocytes and other cell types  Neonatal meningitis- strains possess the K1 capsular antigen ○ Salmonella- Pathogenicity island I encodes salmonella-secreted invasion proteins (Ssps) and a type III secretion system that injects the proteins into the host cell. animal reservoir- poultry, eggs, dairy products, and foods prepared on contaminated work surface ○ Shigella- produce an exotoxin, Shiga toxin= damage to the intestinal epithelium; however, in a small subset of patients, the Shiga toxin can mediate damage to the glomerular endothelial cells, resulting in renal failure (HUS). ○ Yersinia- (1) fraction 1 (f1) gene, which codes for an antiphagocytic protein capsule, and (2) plasminogen activator (pla) protease gene, which degrades complement components C3b and C5a, preventing opsonization and phagocytic migration, respectively. The pla gene also degrades fibrin clots, permitting Y. pestis to spread rapidly. zoonotic, with humans the accidental hosts. There are two forms of Y. pestisinfection: urban plague, for which rats are the natural reservoirs, and sylvatic plague, which causes infections in squirrels, rabbits, field rats, and domestic cats. 3. Outline the medically relevant enterobacteriacea and their clinical syndromes ○ Enterotoxigenic E. coli- Secretory diarrhea, hemorrhagic colitis ○ Salmonella- gastroenteritis, febrile illness called typhoid fever. A milder form of this disease, referred to as paratyphoid fever ○ Shigella- abdominal cramps, diarrhea, fever, and bloody stools ○ Yersinia- Bubonic plague, high fever and a painful bubo (inflammatory swelling of the lymph nodes) , enterocolitis, pseudoappendicitis ○ Klebsiella- lobar pneumonia, donovanosis ○ Proteus- renal (kidney) stones 4. Discuss the laboratory diagnosis of enterobacteriacea ○ sorbitol-containing MacConkey agar (S-MAC), which is used to screen stool specimens for sorbitol-negative (colorless), gram-negative bacteria such as E. coli ○ This cold enrichment permits the growth of Yersinia but inhibits or kills other organisms in the specimen. ○ The treatment paragraphs (consist of 5 paragraphs) indirectly said “well there’s no treatment or vaccine, you're f***ked.”  Infectious Disease 21: Pseudomonas and the related nonfermentative rods 1. Discuss the microbiology characteristics of Pseudomonas and related nonfermentative rods ○ 2. Discuss the virulence factors of Pseudomonas and related nonfermentative rods ○ 3. Outline the medically relevant nonfermentative Gram-Negative rods and their clinical syndromes ○ 4. Discuss the laboratory diagnosis of nonfermentative Gram-Negative bacteria ○ Name Characteristics Clinical manifestations Treatment Pseudomonas -(tracheobronchitis) to combination of severe necrotizing active antibiotics bronchopneumonia -most recognized are Cephalosporins infections of burn wounds (e.g., ceftazidime) -External otitis -primarily opportunistic (i.e., restricted -Corneal ulcers preventing the to patients receiving broad-spectrum -ecthyma gangrenosum contamination of antibiotics that suppress the normal sterile equipment, intestinal bacterial population or patients with compromised host defenses) -Oxidase test= P. aeruginosa -typically arranged in pairs. The grows rapidly and has flat organisms utilize carbohydrates through colonies with a spreading aerobic respiration, with oxygen the border, β -hemolysis, a terminal electron acceptor. green pigmentation caused -presence of cytochrome oxidase by the production of the blue (detected in a rapid 5-minute test) -Exotoxin A- disrupts protein synthesis (pyocyanin) and yellow-green by blocking peptide chain elongation (pyoverdin) pigments, and a -cystic fibrosis- A blue pigment, characteristic sweet, pyocyanin, produced by P. aeruginosa, grapelike odor. catalyzes the production of superoxide and -motility hydrogen peroxide, which are toxic forms  of oxygen. A yellow-green pigment, pyoverdin, is a siderophore that binds iron for use in metabolism. -LasA (serine protease) and LasB (zinc metalloprotease), act synergistically to degrade elastin, resulting in damage to elastin-containing tissues and producing the lung parenchymal damage and hemorrhagic lesions (ecthyma gangrenosum) -Phospholipase C is a heat-labile hemolysin that breaks down lipids and lecithin, facilitating tissue destruction. -Exoenzymes S and T are extracellular toxins produced by P. aeruginosa. When the type III secretion system introduces the proteins into their target eukaryotic cells, epithelial cell damage occurs, facilitating bacterial spread, tissue invasion, and necrosis. Burkholderia -opportunistic pathogens -melioidosis TMX-SMX -​C ​ F or chronic granulomatous -cutaneous infection disease (CGD; a primary -affects pulmonary immunodeficiency in which -cystic fibrosis white blood cells have defective intracellular microbicidal activity) Stenotrophomonas -responsible for infections in -resistant to TMX-SMX maltophilia debilitated patients with carbapenems(e.g., impaired host defense imipenem, meropenem, mechanisms- opportunistic ertapenem, doripenem) Acinetobacter - aerobic, oxidase-negative, plump gram-negative coccobacilli. They are saprophytes -subdivided into two groups: glucose-oxidizing species ( A. baumannii is the most common) and glucose nonoxidizing species ( A. lwoffii and A. haemolyticus are the most common) -opportunistic -Red arrow, blue arrow is pseudomonas Moraxella -strictly aerobic, -bronchitis and resistant to oxidase-positive, gram-negative bronchopneumonia penicillins= diplococci TMX-SMX Infectious Disease 23: Campylobacter and Helicobacter 1. Discuss the microbiology characteristics of Campylobacter and Helicobacter ○ 2. Discuss the pathophysiology and virulence factors for Campylobacter and Helicobacter ○ 3. Outline the clinical syndromes associated with Campylobacter and Helicobacter ○ 4. Discuss the main complications / associations of Campylobacter and Helicobacter Bacteria Characteristics Virulence Factors Clinical Treatment Manifestations Campylobacter -grows better at 42 ° C -(S protein) that prevents -produces Erythromycin or than at 37°C. These properties C3b binding to the bacteria histologic azithromycin have been exploited for the and subsequent damage to the are the antibiotics selective isolation of complement-mediated mucosal of choice for the pathogenic campylobacters in killing in serum. C. fetus surfaces of the treatment of stool specimens loses its virulence if this jejunum (as enteritis - a gram-negative cell wall protein layer is removed. implied by the structure with an outer name of the polysaccharide capsule. species), ileum, and Instead of cell wall colon lipopolysaccharides (LPS) -Guillain-Barré with endotoxin activity found syndrome, which in other gram-negative is an autoimmune bacteria, they express disorder of the lipooligosaccharides. peripheral nervous -are zoonotic, with a variety system of animals serving as characterized by reservoirs (mostly poultry) development of -Gram stain, observation of symmetric the characteristic thin, S weakness over -shaped organisms in a several days and stool specimen recovery requiring months or longer. -antigenic cross-reactivity between the surface lipooligosaccharide s of some strains of Campylobacter and peripheral nerve gangliosides. -Another immune-related late complication of Campylobacter infections is reactive arthritis Helicobacter -spiral gram-negative -tissue damage is mediated -gastritis -combination of a rods resembling by urease by-products , -gastric ulcer proton pump campylobacters were found in mucinase, -duodenal ulcer inhibitor (e.g., patients with type B gastritis phospholipases, and the -gastric cancer omeprazole), a (chronic inflammation of the activity of vacuolating -a monoclonal macrolide (e.g., stomach antrum [pyloric cytotoxin A (VacA), population of B clarithromycin), end]) which is a protein that after cells may develop and a β -lactam -colonize the intestines penetration into epithelial and evolve into a (e.g., amoxicillin) (enterohepatic cells damages the cells by MALT helicobacters) producing vacuoles lymphoma.  - Humans are the primary -The cag p hosphoribosyl a reservoir for H. pylori, nthranilate i somerase and colonization is believed to (PAI) genes also induce persist for life unless the host interleukin (IL)-8 is specifically treated. production,which attracts Transmission is most likely neutrophils. Release of via the fecal-oral route. proteases and reactive oxygen molecules by these neutrophils is believed to contribute to gastritis and gastric ulcers. Infectious Disease 24: Vibrios and Aeromonas 1. Discuss the microbiology characteristics of Vibrio spp and Aeromonas spp ○ 2. Discuss the pathophysiology and virulence factors of Vibrio spp and Aeromonas spp ○ 3. Outline the clinical syndromes associated with Vibrio spp and Aeromonas spp ○ 4. Discuss the complications and associations of Vibrio spp and Aeromonas spp Bacteria Characteristics/ Virulence factors Clinical Manifestations Treatment Vibrio -curved rods - speckled with mucus -treated with fluid -require sodium chloride (“rice-water” stools). The and electrolyte (NaCl) for growth resulting severe fluid and electrolyte replacement -Vibrios tolerate a wide range of loss can lead to dehydration, painful before the pH (e.g., pH of 6.5 to 9.0) but are muscle cramps, metabolic acidosis resultant massive susceptible to stomach acids. -explosive watery diarrhea. fluid loss leads to -polar flagella (important for -primary septicemia (bacteria hypovolemic motility) and various pili that are enter the bloodstream and spread shock. important for virulence throughout the body. It can cause -azithromycin - possess lipopolysaccharides widespread inflammation) , after consisting of lipid A (endotoxin), consumption of contaminated raw core polysaccharide, and an O oysters or rapidly progressive polysaccharide side chain. wound infection after exposure to -O1 and O139 produce cholera contaminated seawater.  toxin and are associated with -tool and wound cultures, including epidemics of cholera. blood agar and MacConkey agar. -accessory cholera Special selective agar for vibrios (e.g., enterotoxin and zonula thiosulfate citrate bile salts sucrose occludens toxin. The [TCBS] agar), as well as an enterotoxin produces increased enrichment broth (e.g., alkaline fluid secretion, and the zonula peptone broth, pH 8.6) occludens toxin loosens the tight junctions (zonula occludens) of the small intestine mucosa, leading to increased intestinal permeability. -complex A-B toxin that is structurally and functionally similar to the heat-labile enterotoxin of enterotoxigenic Escherichia coli (ETEC)= increase cAMP, decrease ATP -a thermostable direct hemolysin (TDH; also called Kanagawa hemolysin )= induces chloride ion secretion in epithelial cells by increasing intracellular calcium. β-hemolytic colonies on agar media with human blood but not sheep blood. These virulent strains are referred to as Kanagawa positive. -grow naturally in estuarine and marine environments Aeromonas -gram-negative, facultative -(1) diarrheal disease in Fluoroquinolones anaerobic, fermentative rod otherwise healthy people, (2) (e.g., that morphologically resembles wound infections, and (3) levofloxacin, members of the family opportunistic systemic ciprofloxacin) are Enterobacteriaceae disease in immunocompromised almost uniformly patients (particularly those with active against hepatobiliary disease or an Aeromonas underlying malignancy). strains isolated in -​​Gastroenteritis typically occurs the United States after the ingestion of and Europe; contaminated water or food (e.g., fresh produce, meats, dairy products) -wound infections most commonly result from a traumatic injury associated with exposure to contaminated water Infectious Disease 25: The Anaerobes - Bacteroidales 1. Discuss the microbiology characteristics of Bacteroidales ○ anaerobic bacteria from intra-abdominal abscesses and systemic infection ○ abundant Gram-negative bacteria ○ they exhibit aerotolerance, which permits survival in the setting of oxygen exposure, conferring microbial adaptability to the extraintestinal environment. ○ 2. Discuss the different types of Bacteroidales and where they are found in the human body ○ human colon 3. Discuss the virulence factors of Bacteroidales ○ Neuraminidase, an enzyme that cleaves terminal sialic acid from host carbohydrates, is required for B fragilis to produce abscesses in an animal model. ○ enteric Gram-negative bacteria synthesize a lipopolysaccharide (LPS) that is endotoxic based on its ability to activate host inflammatory signaling pathways and facilitate immune cell recruitment. The LPS of B fragilis contains a lipid A component that is structurally distinct from E coli LPS, resulting in 100- to 1000-fold lower endotoxicity of B fragilis LPS. ○ capsular polysaccharides that are involved in the attachment of the organisms to the peritoneal tissue and inhibition of complement-mediated  killing, a feature critical to the ability of these bacteria to disseminate. Bacteroides and Parabacteroides species synthesize a large number of capsular polysaccharides polysaccharide A (PSA), is essential for B fragilis to induce abscesses in animal models. The repeating unit of PSA is zwitterionic in that it contains residues with both positive and negative charges. This structural motif induces a host immune response characterized by activation of CD4+ T lymphocytes, which contributes to abscess formation in the peritoneal cavity. ○ B fragilis toxin (BFT) may contribute to the development of colonic cancerous lesions. BFT is a metalloprotease that disrupts the tight junctions of epithelial cells by cleaving E-cadherin, which results in tissue injury and a proproliferative response. 4. Discuss the clinical syndromes associated with Bacteroidales ○ triggers an increase in vascular permeability as a consequence of the host inflammatory response, resulting in the influx of plasma and fibrin deposition. ○ Intra-abdominal abscesses Infectious Disease 26: The Anaerobes - Clostridia 1. Discuss the microbiology characteristics of clostridia ○ Gram-positive, anaerobic, spore-forming rods responsible for several unrelated diseases including pseudomembranous colitis, gas gangrene, cellulitis, tetanus, and botulism “pseudomembranous,” refers to the yellowish plaques composed of fibrin with cellular debris that overlay the ulcerations in the colonic mucosa) ○ large intestine 2. Discuss the different types of clostridia and their virulence factors ○ CLOSTRIDIUM PERFRINGENS- α-toxin, a lecithinase that damages cell membranes, is the toxin most responsible for the symptoms of gas gangrene. Abundant gas is produced by the organism, resulting in crepitus, which can be palpated as small gas bubbles under the skin contaminated food, usually a substance containing meat. The enterotoxin causes diarrhea about 12-24 hours after the contaminated food is eaten. Toxin A (also called TcdA) causes both fluid production and damage to the mucosa of the large bowel. Toxin B is a cytotoxin that causes rounding up of tissue culture cells. Both elicit Glycosylation Rho and Rac making it inactive and the cell loses its cytoskeletal structure and can die as a result ○ CLOSTRIDIUM BOTULINUM - interfering with neurotransmission at peripheral cholinergic synapses. The toxin is a zinc metalloprotease that cleaves proteins involved in the docking of neurotransmitter-filled vesicles with the cytoplasmic membrane of neurons, thereby preventing transmission of the neurological signal to muscles to contract. If infant- (1) the toxin is not found in food but rather is produced in the infant's intestinal tract; (2) the condition has a slow onset, probably because the toxin is absorbed more slowly from the large intestine; and (3) the disease has a favorable outcome in most cases, without specific treatment. ○ CLOSTRIDIUM TETANI AND TETANUS- major toxin, known as tetanospasmin- Several types of neurotransmitters are blocked, including  γ-aminobutyric acid (GABA). Clinically, the disease presents as a spastic paralysis. tetanus are associated with a traumatic wound. Tissue necrosis, anoxia, and other bacterial contaminants in the wound provide an optimal environment for germination of tetanus spores and production of toxin. Neonatal tetanus results from contamination of the umbilical cord at the time of delivery. 3. Discuss the clinical syndromes associated with clostridia ○ CLOSTRIDIUM PERFRINGENS- ulcerating disease of the large bowel known as pseudomembranous colitis (PMC) Treatment- vancomycin and metronidazole ○ CLOSTRIDIUM BOTULINUM - flaccid paralysis of muscle. Cranial nerves are affected first, particularly those involving the eyes, producing diplopia (double vision) and blurred vision. Difficulty swallowing is an early sign. The paralysis descends, and striated muscle groups weaken, especially those in the neck and extremities Treatment= trivalent antitoxin- A, B, E ○ CLOSTRIDIUM TETANI AND TETANUS- trismus, or “lockjaw.” treatment / prevention= Tetanus toxoid is the “T” of the DTaP vaccine