Microbiology - Block 3 - Part 5

davidwurbel7's version from 2015-07-31 15:49


Question Answer
Obligate Aerobic bacilli. Acid-fast bacteria (red). Mycolic acid cell wall. Catalase +. Facultative intracellular. Very fastidious. Very slow (~20hr doubling). Obligate human pathogen. Transmission - Human-to-human aerosol. Resistant to common antibioticsMycobacteria tuberculosis
Mycobacteria tuberculosis appearing as bright red bacilli (rods) in a sputum smear stained withZiehl-Neelsen Stain
Cell wall composed of lipids and thisMycolic Acid
This is based on polypeptides in the cell wallPurified Protein Derivative (PPD)
M. tuberculosis is grown on this blue media on which takes 2-3 weeks to growLowenstein-Jensen (LJ) Media
Typical small, buff coloured colonies on Lowenstein-Jensen medium “ruff, buff & tuff”Mycobacteria tuberculosis
Virulence factor in M. tuberculosis that is thick, hydrophobic barrier protects against free radicals and desiccation. Binds C3b to promote uptake by macrophages, but thick fatty acid layer prevents complement activationMycolic Acid
Virulence factor in M. tuberculosis that is a glycolipid attached to mycolic acids. Forms cords of bacteria. Prevents phagosome fusion with lysosome. Damages mitochondria of neutrophilsCord Factor
Virulence factor in M. tuberculosis that is a mannose core with arabinose side chains. Inhibits macrophage activation and prevents phagosome fusion with lysosomeLipoarabinomannan (LAM)
In primary infection, M. tuberculosis are engulfed by these cell in which M. tuberculosis survives and multiply.Alveolar Macrophages
The fusion of macrophages due to infection by M. tuberculosisLanghans Giant Cell
If bacterial load is high, dendritic cells transport Mtb antigens via lymphatics toHilar Lymph Nodes
Naïve CD4+ T cell are activated and differentiate to Th1 cells which stimulates thisCell Mediated Immune (CMI) Response
Th1 cells migrate to lungs to activate uninfected macrophages and surround the infected macrophages and free bacteriaGranuloma Formation
First exposure. TB skin test negative. X-ray negative. Usually asymptomatic. Usually resolves by producing a calcified granuloma or area of scar tissuePrimary Tuberculosis
TB skin test positive. X-ray positive. Sputum positive. May become symptomaticProgressive Primary Tuberculosis
An asymptomatic chronic state after controlling primary infectionLatent Tuberculosis
Persistent cough with mucous; sometimes with blood. Chest pain. Dyspnea. Weight loss. Night sweats. Fatigue. Low-grade feverPulmonary Tuberculosis
The combination of Ghon focus and Hilar lymph node involvementGhon Complex
A 1-1.5 cm gray white area of caseous necrosis in sub-pleural locationGhon focus (granuloma)
Reactivation of dormant Mtb. Original granuloma bursts or cavitates. Usually at the apex of the lung. Frequently consequence of impaired immunitySecondary Tuberculosis
Chest pain, dyspnea, more sever cough, fever, drenching night sweats, weight loss and hemoptysisSecondary/Reactivation Tuberculosis
Particularly immunocompromised. Can occur after primary exposure or re-activated secondary TB. NOT confined to lungs. Spreads via blood stream in macrophages. Resemble millet seeds. Tubercles found in many tissues. Cancer-like wastingMiliary Tuberculosis
PPD skin test. Chest X-ray. Sputum stain (acid-fast, IF). Sputum cultureTuberculosis Diagnosis
Purified protein derivative administered subdermally. Read in 48-72 hoursMantoux Tuberculin Test (Tuberculosis Test)
Sputum sample or Broncho-Alveolar Lavage (BAL) - 3 consecutive mornings. Stain culture with acid-fast procedure Ziehl-NeelsenM. tuberculosis Sputum Culture
Test quantitates Interferon γ production by pre-sensitized cells. Test is more advantageous for early exposure, immunocompromised or vaccinatedInterferon-gamma Release Assay (IGRA)
Factor that contributes to multiple antibiotic resistanceMycolic Acid
Factor that contributes to TB antibiotic resistanceSlow Growth
Rifampin (RNA Pol), Isoniazid (Mycolic acid), Pyrazinamide (cell membrane & wall), Ethambutol (cell wall)First Two Months Treatment
Rifampin and IsoniazidSecond Four Months Treatment
Ubiquitously found in soil and water. Transmitted by inhaling aerosolized droplets or drinking water. Atypical pneumonia (Lady Windermere Syndrome) in elderly women. Highly disseminated disease in AIDS patients with CD4+ count <50 cells/ul often originating from GI tractMycobacterium avium –intracellulare Complex (MAC)
Targets dermal macrophages and Schwann cells of peripheral nerves. Prefer lower temp. Cannot grow in cell free cultureMycobacteria leprae
High CMI (Th1) response -> Less severe. Formations of granulomas form and control infectionTuberculoid Leprosy
High humoral (Th2) Response -> More severe. Infection is not controlled, resulting in characteristic skin lesionsLepromatous Leprosy
Flat macular lesions consisting of small granulomas with low bacterial numbersTuberculoid Leprosy
Raised papular lesions with no granuloma formation and high bacterial numbers. Loss of eyebrows is characteristic featureLepromatous Leprosy
Branching filaments. Weakly acid-fast, catalase (+) Aerobic. Mycolic acid protects from complement. Cord factor interferes with phagocytic killing. Treatment with Co-trimoxazole (Trimethoprim-Sulfamethoxazole, TMP-SMX)Nocardia asteroids
Almost always in immunocompromised. Cavitations with spread into the pleura with dyspnea, fever & cough. Difficult to differentiate from TuberculosisBronchio-Pulmonary Disease
Branching filaments. Gram +, Anaerobic. Sulfur granules. Clinical presentation with Actinomycosis - Opportunistic Abscess Infections: Pulmonary granuloma formation and Lumpy Jaw abscess. Diagnosis by sulfur granules. Treatment with Penicillin or other beta-lactamsActinomyces israelii
Chronic granulomatous lesions that become suppurate & form abscesses. Bacteria form anaerobic anoxic abscess, which further protects replicating bacteriaActinomycosis
Most common infection. Poor oral hygiene, history of dental disease or oral trauma. Organisms present in mouth invade into diseased tissue & cause disease. Foul smelling with sulfur granulesLumpy Jaw


Question Answer
Infection of lung parenchyma caused by infectious agents that include bacteria, viruses, fungi, and parasitesPneumonia
Inflammation of the bronchi and lungs, usually beginning in the terminal bronchiolesBronchopneumonia
Inflammation of the lungs from a variety of NON-Infectious causes such as chemicals, radiation, autoimmune processesPneumonitis
Inflammation of bronchial tubes. Cause could be viral, bacterial infection and other causes such as irritants like tobacco smoke, air pollution, or chemicalsBronchitis


Question Answer
Most common type of shock with highest mortalitySeptic Shock
Most common type of bacteria that can cause septic shockE. coli
Pathogenesis of septic shock is due to release ofLipopolysaccharides (LPS)
Activation of alternative complement pathway by LPS result in the release of theseC3a and C5a
Direct injury to endothelial cells as a result of C3a and C5a result in the release of these chemical vasodilatorsNO and PG I2
This results in an initial increase in cardiac output, increased MVO2 and decreased peripheral vascular resistanceVasodilation
Clinical features include warm skin, bounding pulse, acute respiratory distress syndrome and disseminated intravascular coagulationSeptic Shock
The first organ to fail in septic shock is usuallyKidneys
Can result in metabolic acidosis, severe absolute neutropenia and disseminated intravascular coagulationShock