Infectious disease p2
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Infectious disease p2

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Infectious disease p2 Infectious disease p2 Presentation Transcript

  • Bacterial InfectionsGRAM-POSITIVE BACTERIAL INFECTIONS :Staphylococcal Infections: Staphylococcus aureus : are pyogenic, nonmotile, Gram-positive cocci that form grapelike clusters. cause skin lesions (boils, carbuncles, impetigo, and scalded skin) and also cause osteomyelitis, pneumonia, endocarditis, food poisoning, and toxic shock syndrome . Staphylococcus epidermidis : causes opportunistic infections in catheterized patients, patients with prosthetic cardiac valves, and drug addicts. Staphylococcus saprophyticus : causes urinary tract infections in young women.
  • Pathogenesis:S. aureus and other virulent staphylococci possessa multitude of virulence factors, which include: surface proteins involved in adherence.secreted enzymes that degrade proteins. secreted toxins that damage host cells.Morphology:Whether the lesion is located inskin, lungs, bones, or heart valves, S. aureus causespyogenic inflammation that is distinctive for its localdestructiveness.
  • Streptococcal Infections: Streptococci are facultative or obligate anaerobic Gram positive cocci that grow in pairs or chains : β-hemolytic streptococci : are typed according to their surface carbohydrate (Lancefield) antigens.• Streptococcus pyogenes (group A) : causes pharyngitis, scarlet fever, erysipelas, impetigo, rheumatic fever, toxic shock syndrome, and glomerulonephritis.• Streptococcus agalactiae (group B) : colonizes female genital tract and causes sepsis and meningitis in neonates and chorioamnionitis in pregnancy.
  •  α-hemolytic streptococcus :• Streptococcus pneumoniae : cause community-acquired pneumonia and meningitis in adults.• Streptococcus viridans : normal oral flora but also cause endocarditis.• Streptococcus mutans : cause dental caries.Pathogenesis: different species of streptococci produce many virulence factors and toxins. Many streptococci, including S. pyogenes and S. pneumoniae have capsules that resist phagocytosis.
  •  S. pyogenes also expresses M protein, a surface protein that prevents bacteria from being phagocytosed. Poststreptococcal acute rheumatic fever is autoimmune disease caused by anti streptococcal M protein antibodies that cross-react with cardiac myosin.Morphology: Streptococcal infections are characterized by diffuse interstitial neutrophilic infiltrates with minimal destruction of host tissues.
  • Diphtheria: Diphtheria is caused by a slender Gram-positive rod with clubbed ends, Corynebacterium diphtheriae, which is passed from person to person through aerosols or skin shedding. C. diphtheriae causes a range of illnesses: asymptomatic carriage ; skin lesions in neglected wounds; and a life-threatening syndrome that includes formation of a tough pharyngeal pseudomembrane ; and toxin-mediated damage to heart, nerves, and other organs. C. diphtheriae has only one toxin which blocks host cell protein synthesis.
  • Morphology: Inhaled C. diphtheriae proliferate at site of attachment on mucosa of nasopharynx, oropharynx, larynx, or trachea. Release of exotoxin causes necrosis of epithelium, accompanied by an outpouring of a dense fibrino suppurative exudate. The coagulation of this exudate on ulcerated necrotic surface creates a tough, dirty gray to black, superficial pseudomembrane. Neutrophilic infiltration in underlying tissues is intense and is accompanied by marked vascular congestion, interstitial edema, and fibrin exudation.
  • Anthrax : Bacillus anthracis is a large, spore-forming Gram-positive rod-shaped bacterium. acquired through exposure to animals or animal products. three major anthrax syndromes: cutaneous, inhalational, and gastrointestinal. Cutaneous anthrax:• painless, pruritic papule that develops into a vesicle within 2 days, and regional lymphadenopathy.• After vesicle ruptures, the remaining ulcer becomes covered with a characteristic black scar.• Bacteremia is rare with cutaneous anthrax.
  •  Inhalational anthrax:• occurs when spores are inhaled, causes hemorrhagic mediastinitis.• Frequently, anthrax meningitis develops due to bacteremia.• Inhalational anthrax rapidly leads to shock and frequently death within 1 to 2 days. Gastrointestinal anthrax:• Uncommon, caused by eating undercooked meat contaminated with B. anthracis.• Initially nausea, abdominal pain, and vomiting.• Severe bloody diarrhea rapidly develops, and mortality is over 50%.
  • Pathogenesis: B. anthracis produces potent toxins and a polyglutamyl capsule that is antiphagocytic.Morphology: Anthrax lesions at any site are typified by necrosis and exudative inflammation with infiltration of neutrophils and macrophages. The presence of large, boxcar-shaped Gram-positive extracellular bacteria in chains, seen histopathologically or recovered in culture, should suggest the diagnosis.
  • Nocardia: aerobic Gram-positive bacteria that grow in distinctive branched chains. In culture, Nocardia form aerial structures with terminal spores, resembling hyphae. Nocardia are found in soil and cause opportunistic infections in immunocompromised people. Nocardia asteroides : causes respiratory infections. Nocardia brasiliensis : infect skin. A fifth of N. asteroides infections involve CNS, presumably after dissemination from lungs.
  • Morphology: The diagnosis of nocardiosis depends on identification of slender Gram-positive organisms arranged in branching filaments . Nocardia stain with modified acid fast stains (Fite-Faraco stain). At any site of infection, Nocardia elicit a suppurative response with central liquefaction and surrounding granulation and fibrosis. Granulomas do not form.
  • GRAM-NEGATIVE BACTERIAL INFECTIONS:Neisserial Infections : Neisseria are Gram-negative diplococci that are flattened on adjoining sides, giving the pair the shape of a coffee bean. These aerobic bacteria grow best on enriched media such as lysed sheeps blood agar ("chocolate" agar). The two clinically significant Neisseria are : Neisseria meningitidis and Neisseria gonorrhoeae. N. meningitidis : cause bacterial meningitis, particularly among people between 5 and 19 years old. N. gonorrhoeae : cause sexually transmitted disease, gonorrhoea.
  • Pathogenesis: Both species of Neisseria use antigenic variation to escape the immune response.
  • Whooping Cough: caused by Gram-negative coccobacillus Bordetella pertussis. is an acute, highly communicable illness characterized by paroxysms of violent coughing followed by a loud inspiratory "whoop." B. pertussis vaccination has been effective in preventing whooping cough.Pathogenesis : B. pertussis colonizes the brush border of bronchial epithelium and also invades macrophages. Pertussis toxin is an exotoxin composed of five distinct peptides.
  • Morphology: Bordetella bacteria cause laryngotracheobronchitis that in severe cases features bronchial mucosal erosion, hyperemia, and copious mucopurulent exudate . a striking peripheral lymphocytosis (up to 90%) with hypercellularity and enlargement of mucosal lymph follicles and peribronchial lymph nodes.
  • Pseudomonas Infection: Pseudomonas aeruginosa is an opportunistic aerobic Gram-negative bacillus that is a deadly pathogen of patients with cystic fibrosis, severe burns, or neutropenia. Most patients with cystic fibrosis die of pulmonary failure secondary to chronic infection with P. aeruginosa. P. aeruginosa also causes corneal keratitis in wearers of contact lenses; endocarditis and osteomyelitis in intravenous drug abusers; external otitis (swimmers ear) in healthy individuals, and severe external otitis in diabetics.
  • Pathogenesis: P. aeruginosa has pili and adherence proteins that bind to epithelial cells and lung mucin. as well as an endotoxin that causes symptoms and signs of Gram-negative sepsis. The organisms also secrete an exotoxin and several other virulence factors.
  • Morphology: Pseudomonas pneumonia: necrotizing inflammation distributing through the terminal airways , with striking whitish necrotic centers and red hemorrhagic peripheral areas. Gram-negative vasculitis accompanied by thrombosis and hemorrhage, although not pathognomonic, is highly suggestive of P. aeruginosa infection.
  • Plague: Yersinia pestis is a Gram-negative facultative intracellular bacterium that is transmitted by fleabites or aerosols. causes a highly invasive fatal systemic infection called plague, also named Black Death. Y. enterocolitica and Y. pseudotuberculosis : are genetically similar to Y. pestis ; these bacteria cause fecal-orally transmitted ileitis and mesenteric lymphadenitis.
  • Morphology: Y. pestis causes lymph node enlargement (buboes), pneumonia, or sepsis, all with striking neutrophilia. The distinctive histologic features of plague include: (1) massive proliferation of organisms. (2) necrosis of tissues and blood vessels with hemorrhage and thrombosis. (3) neutrophilic infiltrates that accumulate adjacent to necrotic areas.
  • Chancroid (Soft Chancre):acute, sexually transmitted, ulcerative infectioncaused by Hemophilus ducreyi.Morphology:Grossly: tender, erythematous papule involving external genitalia. primary lesion erodes to produce an irregular ulcer . In contrast to primary chancre of syphilis, the ulcer of chancroid is not indurated. The regional lymph nodes enlarged and tender in about 50% of cases
  • Microscopically :• the ulcer of chancroid contains a superficial zone of neutrophilic debris and fibrin.• underlying zone of granulation tissue containing areas of necrosis and thrombosed vessels.• A dense, lymphoplasmacytic inflammatory infiltrate is present beneath the layer of granulation tissue.• Coccobacillary organisms are sometimes demonstrable in Gram or silver stains.
  • Granuloma Inguinale:Granuloma inguinale or donovanosis, is a chronicinflammatory disease caused by Calymmatobacteriumdonovani( a minute, encapsulated, coccobacillus ).The organism is sexually transmitted.Morphology:Grossly: a raised, papular lesion involving genitalia. eventually ulceration, and abundant granulation tissue manifested grossly as soft, painless mass. Disfiguring scars in untreated cases. Regional lymph nodes are spared or show only nonspecific reactive changes, in contrast to chancroid.
  • Microscopically: marked epithelial hyperplasia (pseudoepitheliomatous hyperplasia). A mixture of neutrophils and mononuclear inflammatory cells at the base of ulcer and beneath the surrounding epithelium. The organisms are demonstrable in Giemsa-stained smears of exudate as minute encapsulated coccobacilli (Donovan bodies) in macrophages. Silver stains (e.g., Warthin-Starry stain) may also be used.
  • Typical histological pattern showing epithelial proliferation - pseudoepitheliomatoushyperplasia.
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