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Microbial Diseases of the Respiratory System

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  1. Microbial Diseases of the Respiratory System Ch. 24


  3. Table 24.1

  4. Streptococcal Pharyngitis • Also called strep throat • Streptococcus pyogenes • Resistant to phagocytosis • Streptokinases lyse clots • Streptolysins are cytotoxic • Diagnosis by enzyme immunoassay (EIA) tests • Scarlet fever • Erythrogenic toxin produced by lysogenized S. pyogenes

  5. Figure 24.4 Corynebacterium diphtheriae, the cause of diphtheria. Clubbed cells Palisade arrangement

  6. Common cold • Rhinoviruses (50%) • 113 different serotypes • Transmitted by direct contact; but experiments have shown different results • Almost all Rhinoviruses use same receptor protein: Necessary more studies on host-virus attachment in order to get improved treatments

  7. Lower Respiratory System • The ciliary escalator keeps the lower respiratory system sterile. Figure 24.2

  8. Lower Respiratory System Diseases • Bacteria, viruses, and fungi cause • Bronchitis • Bronchiolitis • Pneumonia Streptococcus pneumoniae Mycoplasma pneumoniae Legionella pneumophila • Viral pneumonia • Tuberculosis: Mycobacterium tuberculosis • Pertussis (Whooping Cough):Bordetellapertussis Fungus: Histoplasmosis, Coccidiomycosis, Blastomycosis, Aspergillosis • http://www.youtube.com/watch?v=Hat0_VDQACAPneumonia • http://www.youtube.com/watch?v=HAtu6uNUZyYS. pneumoniae

  9. Tuberculosis • Mycobacterium tuberculosis • Acid-fast rod; transmitted human-to-human • M. bovis: <1% of U.S. cases; not transmitted from human to human • M. avium-intracellulare complex infects people with late-stage HIV infection

  10. Figure 24.8 Mycobacterium tuberculosis. Corded growth

  11. Figure 24.10 A positive tuberculin skin test on an arm.

  12. Diagnosis of Tuberculosis • Tuberculin skin test screening • Purified protein derivative (PPD) tuberculin is a precipitate of molecules obtained from filtrates of sterilized, concentrated cultures • Positive reaction means current or previous infection • Followed by X-ray or CT exam, acid-fast staining of sputum, culturing of bacteria

  13. Treatment of Tuberculosis • Latent infection: • isoniazid (INH) • rifampin (RIF) • rifapentine (RPT) • TB disease: Prolonged treatment with multiple antibiotics (6 to 9 months). (Slow growth) • There are 10 drugs currently approved by the U.S. Food and Drug Administration (FDA) for treating TB. First line drugs:isoniazid (INH); rifampin (RIF); ethambutol (EMB); pyrazinamide (PZA) If resistance occurs: Second line drugs • Vaccines: BCG, live, avirulent M. bovis; not widely used in United States

  14. INFLUENZA VIRUS • GENERAL CHARACTERISTICS • Orthomyxoviridae family • Enveloped-pleomorphic • ssRNA virus • 3 serotypes: A, B, C based on antigens of the protein coat • Most virulent and epidemic spread – Influenza A displaying antigenic variation • Influenza B – more antigenically stable • Incluenza C – minor cause of disease • Segmented genome (8 segments for A, B; 7 for C)

  15. Influenza • Enveloped-ssRNA virus • Hemagglutinin (H) spikes used for attachment to host cells. • Neuraminidase (N) spikes used to release virus from cell. • Envelop: Lipids, prtein, carbohydrate • Spikes: Carbohydrate-protein complexes Figure 24.16

  16. INFLUENZA • Chills, fever, headache, and muscle aches (no intestinal symptoms). • 1% mortality due to secondary bacterial infections. • Vaccine for high-risk individuals.

  17. Treatment • During the 2005--06 influenza season, CDC determined that 193 (92%) of 2009 influenza A (H3N2) viruses isolated from patients in 26 states demonstrated a change at amino acid 31 that confers resistance to amantadines among all tested influenza A (H3N2) and 2009 H1N1 viruses tested . • Therefore, amantadine and rimantadine are not recommended for antiviral treatment or chemoprophylaxis of currently circulating influenza A virus strains. • Source: Morbidity and Mortality Weekly Report (MMWR) (CDC) January 21, 2011 / 60(RR01);1-24 Current treatment: oseltamivir (brand name Tamiflu®) and zanamivir (brand name Relenza® (CDC, 2013)

  18. H7N9 CHINA 2013 H1N1 2009 Mexico Table 24.2

  19. Influenza • Antigenic shift • Changes in H and N antigens evade immunity defenses Probably due to genetic recombination between different strains infecting the same cell • Antigenic drift (Minor annual variations in the antigenic makeup of a strain) (Virus is still Ex. H3N3 but different strains) • Mutations in genes encoding H or N spikes • May involve only 1 amino acid. • Allows virus to avoid mucosal IgA antibodies Annual vaccine - http://www.youtube.com/watch?v=lFl3FRNpU4E&feature=fvw(H1N1) • http://www.youtube.com/watch?v=Rpj0emEGShQ (3.39) (Influenza) (n1n1+ Influenza)


  21. Ch. 25 Microbial Diseases of the Digestive System

  22. The Digestive System Figure 25.1

  23. GASTROINTESTINAL PATHOGENS • CATEGORIES • Ingestion of viable bacteria • Contaminated food or water • Intracellular pathogens - organisms multiply and destroy the intestinal mucosa/submucosa • Extracellular pathogens - organisms multiply and produce toxin • Ingestion of toxins • Disseminated systemic infections • EFFORTS • Establish definitive diagnosis so that source could be found and controlled • Food handlers, carriers

  24. Bacterial Diseases of the Lower Digestive System • Symptoms usually include diarrhea, gastroenteritis, and vomiting • Are treated with fluid and electrolyte replacement. • Infection is caused by growth of a pathogen: • Incubation is from 12 hours to 2 weeks. • Intoxication caused by ingestion of toxin: • Symptoms appear 1 to 48 hours after ingestion

  25. Staphylococcal Food Poisoning Leading cause of gastroenteritis • Heat resistant (60⁰ C) • S. aureusis a facultative anaerobe, gram positive coccus, which appears as grape-like clusters when viewed through a microscope and has large, round, golden-yellow colonies • Coagulase positive (Toxin A, most cases))) or coagulase negative • Toxin produced when food incubated • Toxin heat stable (30 min boiling) (Exception for exotoxins) Figure 25.6

  26. S. aureus

  27. Staphylococcal Food Poisoning • Many persons carry S. aureus in the nasal passages • S. aureus outgrows competing bacteria when food has been cooked: Prepared (cooked) foods that are left at RT (“Temperature abuse”) • Production of toxin A correlates with coagulase enzyme • Also, under high osmotic pressure

  28. Figure 25.6: The sequence of events in a typical outbreak of staphylococcal food poisoning - Overview. Food containing protein is cooked (bacteria usually killed). Then food is contaminated by worker with staphylococci on hands (competing bacteria have been eliminated). Room temperature holding Organisms incubate in food (temp- erature abuse) long enough to form and release toxins. (Reheating will eliminate staphylococci but not the toxin.) Food containing toxins is eaten. Staphylococcal intoxication In 1–6 hours, intoxication occurs.

  29. Cholera • The most serious bacterial disease • Vibrio cholera serotypes that produce cholera toxin. • Exotoxin causes host cells to secrete electrolytes and water • “Rice water stools” • Mortality 50 % when untreated Figure 25.11

  30. Vibrio cholerae • GENERAL CHARACTERISTICS • Facultative • Gram negative, coma shaped • Vibrionaceae • Non-lactose fermenters • Motile strains w/ polar flagellum • Oxidase + • Distinguished from other vibrios by biochemicals and O somatic antigen structure • Strains associated w/ cholera are O:1 w/ three serological variants

  31. Vibrio cholerae • PATHOGENESIS • Carrier: 2 weeks • Acute diarrheal disease caused by enterotoxin (choleragen) • Intestinal colonization & enterotoxin secretion • Disease associated w/ jejunum & colon • Large Infection dose (ID) required to overcome stomach’s acidity • Fatality rates: (epidemics-75%; endemic areas-5-15%) • Transmission associated w/ presence of vibrio in feces or vomits • SPECIMEN/DIAGNOSIS • Stool specimens, rectal swabs • Incubated in Blood agar, MacConkey’s agar, TCBS (thiosulfate-citrate-bile salt-sucrose agar)-alkaline pH (8.5-9.5) • Presence of “rice-water”stools • Serology (slide agglutination tests)

  32. Vibrio cholerae • IMMUNITY • Active • Secretory IgA (prevents attachment) against both O antigen and toxin • Repeated attacks-seldom • TREATMENT • Fluid and electrolyte replacement. • Antibiotics shorten duration of diarrhea (tet, amp, cam and trimethoprim) • CONTROL/PREVENTION • Good sanitation procedures • Immunization w/ bacterial vaccine-limited effectiveness (prepared from either whole cells, LPS, and toxoid)

  33. Escherichiacoli Gastroenteritis • Gram negative, facultative anaerobic rod • Normally harmless, but some strains are pathogenic (contain fimbria) • Occurs as traveler's diarrhea and epidemic diarrhea in nurseries. • 50% of feedlot cattle may have enterohemorrhagic strains in their intestines. • Enterohemorrhagic strains such as E. coli O157:H7 produce Shiga toxin. • O = cell wall antigen • H = flagellar antigen • Similar to Shigella

  34. Clostridium Infections • Gram +, endospore-forming, anaerobic bacillus • Clostridium perfringensGastroenteritis • Grow in intestinal tract, producing Exotoxin • Clostridium difficile–associated diarrhea • Grow following antibiotic therapy • Associated with hospitalized patients and nursing home residents

  35. Helicobacter pylori • Unknown,dismissed as transient till cultured in 1982 from patients (Barry Marshall and Robin Warren) • First classified as Campylobacter (cell morphology) • Later reclassified as Helicobacter • GENERAL CHARACTERISTICS • Gram negative, microaerophilic S-shaped short spirals • Multiple polar flagella (sheathed) • Urease positive • Fastidious

  36. Helicobacter pylori • PATHOGENESIS • Peptic Disease Syndrome (gastritis/stomach & duodenal ulcers) • 75% gastric ulcer patients have documented infections w/ H. pylori • Correlation between high incidence of H. pylori infections and increasing risk of stomach cancer • Symptoms • Nausea, anorexia, vomiting, epigastric pain, low stomach’s acidity • Asymptomatic cases usually occur for decades up to perforated disease • 50 % of world population harbor H. pylori

  37. Helicobacter pylori • RESERVOIR/SOURCE-TRANSMISSION • Resident of surface stomach’s mucosa where mucus protects from stomach’s acidity • Organism’s prevalence due to production of urease that neutralizes stomach’s acidity —> increasing local pH • Method of transmission • Not clearly established. Infections appear to be clustered in families • One study involving clinical staff obtaining a tissue biopsy indicate direct contact (w/ stomach contents)

  38. Helicobacter: Mechanism • Organisms use flagella to penetrate mucosa layer, adhesins (pilus?) to adhere to mucosa • Mucus production decreases as result of toxic effect or body’s inflammatory response • Cytotoxin may be involved-cause vacoulation of gastric epithelial cells (prominent histopathological feature) • Thinning of mucus at infection site —> peptic ulcer of stomach/duodenum Figure 11.12

  39. PATHOGENESIS OF Helicobacter pylori LEADING TO ULCERATION OF THE STOMACH Inflammation causes the access of HCl and pepsins to the mucosa, causing ulcer

  40. Helicobacter pylori • SPECIMEN/DIAGNOSIS • Blood test • Stomach biopsy (a fiberoptic endoscope is introduced into stomach through mouth and pinches off small piece of stomach lining) • Organisms grow after 2-5 days on enriched media under microarophillic conditions (increasing CO2, humidity) • Breath Test - Radioactively labeled urea is swallowed and detection of radioactively labeled CO2 in patient’s breath w/in 30 min • https://www.youtube.com/watch?v=mw8ptO3Ty6A

  41. Helicobacter pylori • Increased risk of cancer • TREATMENT • Combination of bismuth salts (Bismuth subsalicylate-Pepto-Bismol) • Antibiotic treatment - metronidazole, tetracycline or amoxicillin • Treatments leads to disappearance of peptic ulcer • Recurrence rate – low

  42. Hepatitis • *Berlin, Germany, April 2011: Data from phase I trials of an HCV vaccine presented at the International Liver CongressTM show encouraging results, with high immunogenicity and good safety profile.1,2 • Australia, Aug. 2012: Another promising candidate • December 2013: Still no commercial vaccine available (CDC)

  43. Figure 25.16: Hepatitis B virus (HBV). (3 of 4) Envelope (HBSAg) Spikes Capsomere DNA Dane particle (complete HBV)

  44. Shigellosis (Bacillary Dysentery*)

  45. Salmonellosis • Gram Negative, facultative • Fever, nausea, diarrhea • Low mortality • Treatment: Rehydratation • S. typhimurium Figure 25.9

  46. Typhoid Fever • Caused by Salmonella typhi • Bacteria spread throughout body in phagocytes • High fever, significant mortality • 1–3% of recovered patients become chronic carriers

  47. Salmonellosis and Typhoid Fever Figure 25.10

  48. Campylobacter Gastroenteritis

  49. Ch. 21 Microbial Diseases of the Skin and Eyes