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186 Cards in this Set
- Front
- Back
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manifestation of prions?
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spongiform encephalopathies
(kuru, Creutzfeldt-Jakob dz, BSE, variant CJD) |
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what are silver stains used to ID?
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fungi, legionellae, pneumocystis
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what is PAS used to ID?
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fungi, amebae
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what is mucicarmine used to ID?
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cryptococci
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what is the Giemsa stain used to ID?
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campylobacteria, leishmaniae, malaria, parasites
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what defenses prevent organism entry through the skin?
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keratinized layer, low pH, presence of fatty acids
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what are the normal defense mechanisms of the GI tract?
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layer of viscous mucus, lytic pancreatic enzymes and bile detergents, mucosal antimicrobial peptides, normal flora, secreted IgA
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what type of viruses are resistant to bile and digestive enzymes?
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non-enveloped viruses
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what is the mechanism of gastrointestinal disease of staphylococci?
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enterotoxins released in contaminated food
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what is the mechanism of gastrointestinal disease of V. cholerae and ETEC?
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Vibrio cholerae. Comma shaped. Gram negative. 140 serotypes.
multiply inside mucous layer overlying gut epithelium and release exotoxins that cause epithelium to secrete large amts of fluid Faecal-oral transmission. Flagellae result in penetration of mucous layer Multiply underneath the mucous layer Remain in the lumen and secrete enterotoxin – cholera toxin – very similar to E. coli enterotoxin. Cholera toxin results in persistent activation of adenylate cyclase, high levels of intracellular cAMP and massive secretion of chloride, sodium, bicarbonate and water. No invasion therefore minor histopathological changes. Rice water stool. |
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what is the mechanism of gastrointestinal disease of Shigella, Salmonella, and Campylobacter?
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invade and damage intestinal mucosa and lamina propria and cause ulceration, inflammation and hemorrhage --> dysentery
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what is the mechanism of gastrointestinal disease of Salmonella typhi?
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passes from damaged mucosa thru Peyer patches and mesenteric LNs and into blood, resulting in systemic infection
Samonella typhi – protracted illness characterised by fever, rash and profuse bloody diarrhoea. Hepatosplenomegaly is common. Gallbladder colonization may result in a carrier state. |
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what is the mechanism of respiratory disease of influenza virus?
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hemagglutinin proteins bind to sialic acid on epithelial cells, which leads to phagocytosis where the virus replicates, then neuraminidase cleaves sialic acid to release it from the cell
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which bacteria can impair respiratory ciliary activity?
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H. influenzae, Bordetella pertussis, M. pneumoniae
(P. aeruginosa can cause infxn in pts with CF) |
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infections common in pts with CF?
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respiratory infxns with P. aeruginosa, S. aureus, Burkholdaria cepacia
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granulomatous inflammation is usually evoked by what type of infectious agents?
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ones that resist eradication and are ca[pable of stimulating strong T cell-mediated immunity
E.g. M. tuberculosis, Histoplasma, schistosome eggs |
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acute diffuse mononuclear interstitial inflammation is often a response to what?
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viruses, intracellular bacteria or intracellular parasites
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what characterizes cytopathic-cytoproliferative reactions and what is the usual cause?
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cell necrosis or cellular proliferation, usually with sparse inflammatory cells
Proliferation of epithelial cells can cause warty lesions Viruses can cause dysplastic changes |
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mechanisms of immune evasion?
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1. growth in inaccessible areas
2. antigenic variation 3. resistance to innate immune defenses 4. impairment of effective T cell antimicrobial responses |
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what characterizes necrotizing inflammation and what is the usual cause?
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severe tissue necrosis w/o inflammation
caused by rampant viral infection (fulminant HBV), secreted bacterial toxins (C. perfringens), or direct protozoan cytolysis of host cells (E. histolytica) |
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what viruses are specific to the respiratory tract?
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adenovirus
rhinovirus influenza A/B RSV |
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what viruses are specific to the GI tract?
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mumps
rotavirus norovirus hepatitis A-E |
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what viruses are systemic w/ skin eruptions?
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measles
rubella VZV HSV1/2 |
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what viruses are systemic with hematopoeitic disorders?
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CMV
EBV HIV1/2 |
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what are the species of arboviral and hemorrhagic fevers
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dengue virus
yellow fever virus |
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what viruses cause skin/genital warts?
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papillomavirus
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what viruses are specific to the CNS?
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poliovirus
JC virus |
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cell surface receptors of measles (rubeola)?
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CD46 (complement regulatory protein that inactivates C3 convertases)
SLAM (involved in T-cell activation) |
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blotchy, red-brown rash on face, trunk, limbs; ulcerated mucosal lesions in mouth near Stensens duct; follicular hyperplasia and germinal centers in lymph organs; multinucleated cells w/ eosinophilic nuclear and cytoplasmic inclusion bodies?
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Measles (rubeola)
(paramyxovirus) |
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B/L enlarged parotid glands; possible involvement of testes, pancreas, CNS; lesions show interstitial edema, diffuse macrophage, lymphocyte, and plasma cell infiltrates?
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Mumps
(paramyxovirus) |
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usually asxs, but can invade CNS, replicate in motor neurons of spinal cord or brain stem, causing muscular paralysis or respiratory paralysis?
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Poliovirus
(unencapsulated RNA enterovirus) |
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What is an arbovirus?
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arthropod-borne virus
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birds are major reservoir; usually asxs, but 20% mild fever, HA, myalgia, 50% maculopapular rash; carries risk of CNS complications w/ acute flaccid paralysis; CCR5 is essential for host immune defense
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West Nile virus
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infxns w/ fever and hemorrhage; wide range of presentations from fever, HA, myalgia, rash, neutropenia, thrombocytopenia to severe hemodynamic deterioration; usually infect endothelial cells
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Viral hemorrhagic fevers
(enveloped RNA viruses: arenavirus, filovirus, bunyavirus, flavivirus) |
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replication in skin and mucous membranes at site of entry causes vesicular lesions; lesions show multinucleated cells with pink-purple intranuclear inclusions visible on Tzanck smear?
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Herpes simplex virus- DS DNA virus
Spread by body fluids Replicate in the skin and mucous membranes. Cause primary and recurrent infections. Primary infection resolves after a few weeks but virus remains latent in neurons. Reactivation may occur repeatedly with or without symptoms. May causes conjunctivitis and corneal infection, and encephalitis. |
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which viruses are the α-group chronic latent infections?
what cells infected? |
HSV 1/2, VZV
infect epithelial cells and latent infxn in neurons |
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what are the lymphotropic β-group viruses?
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CMV, Human herpes virus 6 (causes exanthem subitum), Human herpes virus 7
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what are the γ-group viruses?
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EBV, KSHV (HHV-8; cause of Kaposi sarcoma)
Latent virus is in lymphoid cells |
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infxn with rash starting on trunk, spreading to head and limbs, progresses rapidly from macule to vesicle?
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VZV
latent virus in sensory ganglia Droplet spread VZV infects mucous membranes, skin and neurons Disseminates haematogenously In neurons, primarily infects dorsal root ganglia and can be reactivated years later to result in shingles Usually reactivates in elderly or immunocompromised |
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latently infect monocytes, reactivated when immunity is depressed; asxs or mononucleosis-like infxn in normal pts, severe systemic infxn in neonates and immunocompromised; cells are large w/ large purple inclusions surrounded by clear halo
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CMV
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most common opportunistic pathogen in AIDS pts?
how does it manifest in these pts? |
CMV
mononucleosis-like illness: fever, atypical lymphocytosis, lymphadenopathy, hepatomegaly, mild hepatitis |
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how does CMV avoid host defenses?
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downmodulating MHC I and II moelcules and producing homologues of TNF receptor, IL-10 and MHC I molecules
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what determines whether a person will resolve or be a carrier after HBV infection?
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the effectiveness of the CTL response
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benign lymphoproliferative dz w/ fever, sore throat, lymphadenopathy, splenomegaly, increased WBC (especially large, atypical lymphocytes); B-cells are reservoir of latent infxn; may be associated with B-cell lymphoma in immunocompromised
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EBV
EBV transmitted via saliva. Virus penetrates upper respiratory tract epithelial cells and B cells. Infection results in immune response including humoral and cellular response. Cytotoxic T cell form atypical lymphocytes which are typical of the disease. Latent EBV remains in B cells and is linked with later development of Burkitts lymphoma. |
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EBV-associated Burkitt lymphoma is associated with what mutation?
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translocation of the c-myc oncogene into the immunoglobulin heavy chain region
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pyogenic, G+ cocci; grow in clusters
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staphylococci
Surface molecules - bind to endothelial cells, extracellular matrix and artificial materials and increase adherence. Secreted enzymes - lipase degrades skin lipids and allows tissue invasion. Production of toxins Haemolytic toxins including alpha, beta, delta and gamma toxins that cause cell disruption and lysis. Enterotoxins Food poisoning – toxin stimulates vomiting centres in GIT. Enterotoxin also acts as a ‘Superantigen’ – atypical binding to MHC II causes massive stimulation of T cell and release of cytokines that cause systemic effect. Exfoliative toxins – cells in granular layer of epidermis detach from each other – scalded skin syndrome. Toxic shock syndrome toxin – resembles enterotoxin in effect and causes massive release of cytokines |
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what are the virulence factors of S. aureus?
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surface proteins that allow binding to host endothelial cells
polysaccharide capsule resist phagocytosis enzymes that degrade host proteins (lipase - skin abscesses, protein A binds Fc on Ig's to avoid Ab-mediated killing) Hemolysins (damage membranes) Exfoliative toxins (induce skin sloughing by degrading desmoglein 1 which holds epidermal cells together) Enterotoxins (vomiting) Superantigens (shock) |
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what kind of pts do less virulent staphylococci infect?
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catheterized pts, pts w/ prosthetic heart valves, or IV drug abusers (S. epidermidis)
Urinary tract infections (S. saprophyticus) |
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facultative or obligate anaerobic G+ cocci growing in pairs or chains; cause suppurative infxns of skin, oropharynx, lungs, and heart valves
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Streptococci
Common cause of skin and respiratory infections, endocarditis and post- streptococcal immune mediated syndromes such as GN, rheumatic fever and erythema nodosum |
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how are β-streptococci classified?
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according to their CHO (Lancefield) antigens
Beta haemolytic Group A – streptococcus pyogenes Group B – streptococcus agalactaie Group D - enterococcus faecalis Streptococcus pneumoniae Alpha haemolytic Streptococcus viridans |
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what are the β-streptococci?
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S. pyogenes (Group A)
S. agalactiae (Group B) |
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pathogen that causes pharyngitis, scarlet fever, erysipelas, impetigo, RF, TSS, glmerulonephritis
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S. pyogenes
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pathogen that colonizes female GU tract, causes sepsis and meningitis in neonates and chorioamnionitis in pregnancy
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S. agalactiae
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what are the α-streptococci?
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S. pneumoniae
S. viridans group |
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pathogen that is common cause of adult community-acquired pneumonia and meningitis
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S. pneumoniae
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pathogen that is normal oral flora, causes dental caries and endocarditis
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S. viridans (S. mutans = caries)
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Pathogens that are often abx resistant and cause endocarditis and UTIs
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Enterococci
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Special virulence factors of S. pyogenes?
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M protein (prevents bacteria from phagocytosis)
C5a peptidase (degrades chemotactic complement) Pyrogenic exotoxin (causes fever and rash in scarlet fever) |
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Virulence factor of S. pneumoniae?
Virulence factors for strep in general? |
Pneumolysin (cyosolic bacterial protein released on cell disruption which lyses host cell membranes and activates classical pathway of complement activation)
Capsule – pneumococci have a polysaccharide capsule that prevents phagocytosis. Surface molecules – M protein inhibits phagocytosis, lipoteichoic acid binds to extracellular matrix. Secreted enzymes – C5a peptidase degrades C5a, pneumolysin inserts into target cell membranes and lyses them (and also activates complement, making less complement available for bacterial lysis). Production of toxins Pyrogenic exotoxin – causes fever and rash in scarlet fever, erysipelas. Rheumatic fever results from production of anti M protein antibodies that cross-react with cardiac myosin. |
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How does S. mutans cause caries?
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metabolizes sucrose to lactic acid and secretes HMW glucans that promote bacterial aggregation
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what differentiates infxns by Staph and Strep?
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diffuse interstitial neutrophilic infiltrates w/ MINIMAL host tissue destruction
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G+ rod w/ clubbed ends that causes disease characterized by durable membrane at the site of growth in oropharynx, exotoxin-mediated damage to heart, nerves, and other organs
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C. diptheriae
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necrosis of epithelium by this pathogen causes production of a dense fibrinosuppurative exudate resulting in a tough, dirty gray to black, superficial membrane in airway
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C. diptheriae
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virulence factor of C. diphtheriae?
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phage-encoded A-B toxin
B binds cell and allows entry of A A inactivates EF-2 via ADP-ribosylation, blocking protein synthesis release of toxin in pharynx causes epithelial necrosis w/ fibrinosuppurative exudate |
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Is there immunization against C. diphtheriae?
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Yes, but does not protect against infxn, only against lethal effects
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G+ facultative intracellular rod; food-borne sepsis and meningitis in elderly and immunosuppressed, placental infections, granulomatosis infantiseptica; identified by finding bacteria in CSF, exudative inflammation w/ neutrophils.
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Listeria monocytogenes
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virulence factors of L. monocytogenes?
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bind to E-cadherin on epithelial cells and are internalized; use listeriolysin O and two phospholipases to escape phagolysosome; ACTA induces actin polymerization to propel bacteria into adjacent cells
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what can happen with Listeriosis in pregnant women?
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amnionitis which can cause abortion, stillbirth or neonatal sepsis (granulomatosis infantiseptica)
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what macrophage activator is crucial to killing of L. monocytogenes?
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IFN-γ
(IFN-γ-activated macrophages kill phagocytosed listeria, C3-activated macrophages do not) |
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Spore-forming G+ rod common in animals that have had contact with contaminated soil; lesions exhibit necrosis w/ neutrophils and macrophages and large, boxcar-shaped extracellular bacteria in chains
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B. anthracis
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Syndromes produced by anthrax?
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Cutaneous: painless, pruritic papules --> edematous vesicles --> black eschar
Inhalational: release of toxins causes hemorrhagic mediastinitis; prodromal fever, cough, and chest/abd pain rapidly leads to sepsis, shock, death GI: n/v, abd pain --> severe, bloody diarrhea, death |
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Virulence factors of anthrax?
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A-B toxin: B = protective factor (binds host cell)
A = edema factor (converts ATP to cAMP --> water efflux) or lethal factor (protease that kills cells by destroying mitogen-activated protein kinase kinases) |
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aerobic, G+, grows in branched chains; cause opportunistic indolent respiratory infxn w/ CNS dissemination mostly in pts T-cell immune deficiency
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Nocardia asteriodes
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pathogen that causes indolent illness with fever, weight loss, and cough; arrange in branching filaments, stain with modified acid-fast stains; sites of infection have suppurative response with central liquefaction and surrounding granulation and fibrosis (w/o granulomas)
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Nocardia asteroides
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Major aerobic G- bacterial infections
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Neisseria
Whooping cough (B. pertussis) Pseudomonas aeruginosa Plague (Yersinia pestis) Chancroid (Hemophilus ducreyi) Granuloma inguinale (Klebsiella granulomatis) |
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small, G- aerobic diplococci; cause suppurative, bacterial meningitis esp in <2 y.o., invasive dz occurs in crowded conditions
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Neisseria meningitidis
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What confers increased risk of Neisseria meningitis?
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C5-C9 complement deficiencies
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In males, causes symptomatic urethritis; in females, often asxs, can lead to PID; in neonates, can cause blindness; usually manifests in genital or cervical mucosa, pharynx or anorectum
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N. gonnorhoeae
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Prevention of gonorrheal blindness in neonates?
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otic drops of silver nitrate or antibiotics
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Neisseria: mechanism of immune evasion?
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antigenic variation of surface attachment proteins (pili proteins and OPA proteins)
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disseminated infection of this pathogen causes septic arthritis accompanied by a rash of hemorrhagic papules and pustules
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N. gonorrhoeae
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G- coccobacillus that causes a laryngotracheobronchitis that causes bronchial mucosal erosion, hyperemia and copious mucopurulent exudate w/ peripheral lymphocytosis resulting in violent paroxysms of coughing
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Bordetella pertussis
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Virulence factors of B. pertussis?
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virulence factors coordinated by BVGS transmembrane protein; pertussis toxin ADP-ribosylates and inactivates guanine nucleotide-binding proteins, resulting in failure in transmitting signals from host plasma membrane receptors thus paralyzing cilia.
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Opportunistic, aerobic G- bacillus; frequently seen in CF, burns, or neutropenia; in neutropenic pts, can cause extensive necrosis by vascular invasion w/ subsequent thrombosis
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P. aeruginosa
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virulence factors of P. aeruginosa?
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Pili and adherence proteins (bind to epithelial cells and lung mucin)
Endotoxin Exotoxin A (inhibits protein sythesis by ADP-ribosylating EF-2) Exoenzyme S (ADP-ribosylates RAS and G proteins that regulate cell growth and metabolism) Alginate (forms slimy biofilm to protect it from Ab, complement, phagocytes, and abx) |
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Which bacteria use exotoxin A?
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Corynebacterium diphtheriae and Pseudomonas aeruginosa
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Necrotizing pneumonia in terminal airways in a fleur-de-lis pattern with pale centers and red, hemorrhagic peripheral areas along with G- vasculitis w/ thrombosis and hemorrhage suggests what pathogen?
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P. aeruginosa
Opportunistic gram negative organism, important cause of morbidity and mortaility in cystic fibrosis, burns, neutropenia Third most common cause of hospital acquired infection Corregated pili and adherance proteins mediate adherance to epithelial cells Colonies secrete a alginate covering that protects them from phagocytosis Secrete exotoxin A that is similar to diphtheria toxin Secrete enzymes that inhibit host cell growth, lyses red cells, degrades surfactant and degrades extracellular matrix Secretes toxic iron containing compounds that damage endothelial cells |
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G- facultative intracellular bacteria that proliferate in lymphoid tissue; cause ileitis, mesenteric lymphadenitis, pneumonia, sepsis w/ neutrophilia
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Yersinia (pestis, enterocolitica, pseudotuberculosis)
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Acute, ulcerative genital infxn, most common in Africa and SE Asia
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Chancroid (Hemophilus ducreyi)
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histological appearance of ulcer formed by chancroid?
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contains neutrophils and fibrin w/ underlying zone of granulation tissue, necrosis, and thrombosis and lymphoplasmacytic infiltrate
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sexually transmitted minute, encapsulated coccobacillus; endemic in tropical and subtropical regions; untreated leads to scarring, associated with lymphatic obstruction and elephantiasis of external genitalia
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Klebsiella granulomatis (Granuloma Inguinale)
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slender, aerobic, acid-fast rods growing in straight or branching chains
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Mycobacterium
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what increases the risk of Tb?
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poverty, overcrowding, chronic debilitating illness, diabetes, Hodgkin lymphoma, chronic lung dz (particularly silicosis), chronic renal flr, malnutrition, alcoholism, immunosuppression
Infects one third of world population Kills 3 million per year. |
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When will PPD detect active Tb infection?
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2-4 wks after initial infection
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what does a positive PPD indicate?
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pt has T cell-mediated immunity to mycobacterial antigens; does not differentiate between infection and disease
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causes of false negatives in PPD?
causes of false positives in PPD? |
False Neg: some viral infxns, sarcoidosis, malnutrition, Hodgkin lymphoma, immunosuppression, overwhelming active Tb disease
False Pos: infxn by atypical mycobacteria, prior vaccination with BCG |
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What are the primary cells infected by M. tuberculosis?
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Macrophages
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Progression of normal M. tuberculosis infxn?
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1. bacteria enter macrophages because macrophages bind bacterial lipoarabinomannan
2. bacteria block phagosome-lysosome fusion and proliferate 3. 2-4 wks after infxn, T cells specific to M. tuberculosis proliferate and make IFN-γ 4. IFN-γ activates macrophages to kill bacteria via N2O synthase |
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what are the characteristic pathologic manifestations of Tb?
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caseating granulomas and cavitation
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Fosamax
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Alendronate
a-LEN-droe-nate |
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what is "secondary" Tb?
how is it characterized? |
pattern of dz arising in a previously sensitized host;
insidious onset of wt loss, low grade fever, and night sweats; increasing amts of mucoid to purulent sputum, 50% have hemoptysis |
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What is the Ghon complex? With what is it associated?
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lung and draining lymph node granulomas
associated with primary Tb |
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what manifestation of Tb is more common in advanced HIV?
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extrapulmonary involvement
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Common environmental bacteria causing widely disseminated infxn characterized by abundant acid-fast organisms in macrophages of immunocompromised hosts?
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M. avium-intracellulare Complex
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What is the result of systemic arterial dissemination of M. tuberculosis to peripheral organs, meninges, and bone marrow?
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Systemic miliary tuberculosis
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slowly progressive infxn that affects skin and peripheral nerves (due to bacteria growing only in cooler tissues of the periphery); results in disabling deformities?
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Leprosy (M. leprae)
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Insidious infxn leading to dry, scaly skin lesions lacking sensation, w/ asymmetric peripheral nerve involvement; on microscopy, few bacteria are found?
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Tuberculoid leprosy
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Systemic infxn with disfiguring cutaneous thickening and nodules, w/ nervous system damage d/t bacterial invasion into perineural macrophages and Schwann cells; on microscopy, aggregates of lipid-laden macrophages and abundant bacteria?
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Lepromatous (anergic) leprosy
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What determines which kind of leprosy an infected individual will have?
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T-helper lymphocyte response
(tuberculoid = Th1 cells make IL-2 and IFN-γ; lepromatous = weak Th1 response followed by ineffective Th2 response) |
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neuronal involvement dominates which type of leprosy?
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Tuberculoid
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G-, slender corkscrew-shaped bacteria with axial periplasmic flagella?
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Spirochetes
Treponema pallidum Spirochaete detectable by silver stain, darkfield examination and immunofluoescense |
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Infxn characterized by development of firm, nontender, raised red lesion on site of infxn 3 wks after inoculation; bacteria are present in the lesion and exudate has infiltrate of plasma cells, macrophages, lymphocytes and proliferative endarteritis
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Primary syphilis
3 weeks after contact. Single, firm, raised, red, non-tender chancre at site of invasion. Chancre heals spontaneously. |
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5-13 wks after inoculation, cutaneous spread of this pathogen causes maculopapular, scaly or pustular lesions on the palms or soles of feet, condylomata lata, and silvery-gray erosions of mucous membranes, all of which are painless; also lymphadenopathy, mild fever, malaise, wt loss
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Secondary syphilis
2-10 weeks after primary chancre. Palmer/solar rash, fever, lymphadenopathy, headache, arthritis. |
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chronic infection that can cause aortic valve insufficiency and aortic aneurysms, chronic meningovascular dz, tabes dorsalis, general paresis; increased inflammatory cells, protein, or decreased glucose in CSF
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Tertiary syphilis
Neurosyphilis – paresis, meningovascular, tabes dorsalis Aortitis – aneuryms, aortic regurgitation. Gummas – liver, bones and skin. Congenital syphilis Typically causes stillbirth, skin sloghing, saber shin, liver and lung (plus other organs) fibrosis, keratitis, Hutchinson teeth, eighth nerve lesions |
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Disease associated with necrotic, rubbery masses which form in bone, skin and oral mucosa
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Benign tertiary syphilis
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Risks associated with congenital syphilis?
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intrauterine death, perinatal death, nasal discharge and congestion, sloughing of the skin, hepatomegaly, skeletal abnormalities
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When can VDRL and RPR detect syphilis infection?
When do they become negative? |
4 to 6 wks after infection
Tertiary syphilis |
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What is the best test for detection of early syphilis infection?
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immunofluorescence of chancre exudate
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what sx is seen in all stages of syphilis?
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endarteritis (inflammation of arterial inner lining; endothelial cell activation and proliferation --> intimal fibrosis)
Treponemes bind to endothelial cells and cause an obliterative endarteritis followed by delayed hypersensitivity. Host humoral and cellular response is insufficient to clear the spirochaetes – either due to poor antigenic stimulus or direct down-regulation of CD4 cells. |
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the triad of interstitial keratitis, Hutchinson teeth, and 8th nerve deafness are the late manifestations of what disease?
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congenital syphilis
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What pathogen is transmitted by body lice or ticks and is clinically manifested by shaking chills, fever, HA, and fatigue, followed by DIC and multi-organ failure?
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Borrelia recurrentis (relapsing fever)
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what pathogen causes an erythematous papule with a pale center with fever and lymphadenopathy during the acute phase; skin lesions, migratory arthralgias and myalgias, arrhythmias and meningitis during the second stage; and chronic, destructive arthritis and encephalitis in the late chronic stage?
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Lyme disease (Borrelia burgdorferi)
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what is the usual cause of abscesses?
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commensal bacteria from adjacent sites, usually anaerobic>aerobic
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G+, anaerobic bacilli that cause cellulitis and myonecrosis of wounds, food poisoning and small bowel infection?
C.diff mechanism? |
Clostridium perfringens, C. septicum
Clostridium difficile Normal inhabitant of gastrointestinal tract that proliferates if antibiotics reduce other flora. Secreted toxins cause local bowel damage (toxin A is an enterotoxin and granulocyte chemoattractant, toxin B causes cytopathic effects) characterized by fibrinous pseudomembranes. |
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this pathogen proliferates in wounds and causes spastic paralysis
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Clostridium tetani
Uncommon due to immunization and education. Common in undeveloped nations especially neonatal tetanus. Transmission most commonly occurs from soil-contaminated wounds. Clostridium tetani neurotoxin – Extremely potent toxin Binds to gangliosides on peripheral nerves, transported to the nucleus via the axon, is released from the nucleus to be taken up by inhibitory neurons where it cleaves synaptobrevin, destroying the ability of inhibitory synaptic vesicles to fuse. |
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MOA of tetanospasmin?
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blocks release of GABA
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pathogen that grows in canned foods and releases a toxin that blocks release of ACh leading to repiratory and skeletal paralysis
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Clostridium botulinum
Uncommon due to controls on heat processing of food. Spores are heat resistant and and are able to survive in improperly heat-processed foods to cause food poisoning. Results from ingestion of preformed toxin. Clostridium botulinum neurotoxin Acts at peripheral nerve endings, cleaves synaptobrein, SNAP 25 and syntaxin, prevents vesicles from fusing. Mostly affects NMJ and autonomic system. |
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important toxin of C. perfringens and MOA?
Cellulitis and gas gangrene Uncommon due to wound management procedures and antibiotics |
α-toxin
degrades lecithin (component of cell membranes), thus destroying RBCs, PLTs, muscle cells, can also cause nerve sheath damage Infection usually results from traumatic injury and contaminated wound. Clostridium perfringens is able to produce various enzymes (collagenase and hyaluronidase degrade extracellular matrix) and toxins able to destroy tissue within anerobic wounds |
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MOA of botulinum toxin?
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blocks synaptobrevin which mediates fusion of NT-vesicles with neuron membrane, thus preventing ACh release at the neuromuscular junction
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small, G- obligate intracellular bacteria that may be asxs or may cause urethritis, epididymitis, prostatitis, PID, pharyngitis, conjunctivitis, perihepatic inflammation and proctitis
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Chlamydia trachomatis
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which serotypes of chlamydia cause urogenital infections and inclusion conjunctivitis?
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D through K
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which serotypes of chlamydia cause lymphogranuloma venereum (chronic, ulcerative disease in Asia, Africa, Caribbean and S. America)?
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L1, L2, and L3
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which serotypes of chlamydia cause trachoma (ocular infection of children)?
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A, B, and C
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G-, intracellular bacilli that cause epidemic typhus, scrub typhus erlichiosis and spotted fever?
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Rickettsiae
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Type of Rickettsial infxn with lesions that range from a rash w/ small hemorrhages, to skin necrosis and gangrene w/ internal organ hemorrhages
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Epidemic typhus (R. prowazekii)
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Pathogens that predominantly infect vascular endothelial cells causing vascular leakage from endothelial damage, resulting in hypovolemic shock w/ peripheral edema, pulmonary edema, renal failure and CNS manifestations
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Rickettsiae
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which organisms proliferate in endothelaila cells, causing endothelial swelling, thrombosis and vessel wall necrosis (manifesting as gangrene of tips of fingers, nose, earlobes, scrotum, penis and vulva), w/ a perivascular cuff of mononuclear inflammatory cells?
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Typhus and spotted fever (Rickettsiae)
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What disease is caused by infection of neutrophils or macrophages and manifests as fever, HA, malaise, progressing to respiratory insuff., renal failure, and shock?
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Erlichiosis (Rickettsiae transmitted by ticks)
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this infxn causes a hemorrhagic rash over the entire body, including palms and soles, and is common in SE and south-central US?
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Rocky Mountain Spotted Fever (Rickettsia rickettsii)
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candida produces what diseases in healthy ppl?
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vaginitis and diaper rash
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who is susceptible to superficial candidiasis?
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burn victims, diabetics
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fungus that is spore at 20degC, forms germ tubes at 37degC; pseudohyphae
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candida
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heavily encapsulated monomorphic yeast that causes meningitis that appear as soap-bubble lesions in the brain; found in soil, pigeon droppings
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cryptococcus
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mold that causes pulmonary allergy in healthy ppl, serious sinusitis, pneumonia and invasive dz in IC; septate hyphae branching at acute angles
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aspergillus
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Mold with irregular nonseptate hyphae branching at wide (90+ deg) angles; cause dz in ketoacidotic diabetics and leukemic pts
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mucor
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intracellular protozoa that causes cyclic fever, anemia, cerebral sxs, renal flr, pulmonary edema, splenomegaly; first invades hepatocytes, then ruptures and infects RBCs
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Plasmodium
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protozoa that parasitizes RBCs and causes fever and hemolytic anemia; transmitted by ixodes tick; in RBC, has ring stages, Maltese cross
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Babesia
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intracellular protozoa transmitted by sandfly; causes chronic inflammatory dz of skin, mucous membranes; visceral dz has spiking fevers, hepatosplenomegaly, pancytopenia; macrophages contain amastigotes
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leishmania
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extracellular protozoa that cause recurring fever, enlarged LNs, splenomegaly and progressive brain dysfxn --> death; red-rubbery chancre at site of insect bite
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Trypanosoma
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intracellular protozoa that uses cell lysosome to activate; causes dCM, megacolon, megaesophagus, predominantly in S. America
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Chagas dz (Trypanosoma cruzi)
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Nematode whose larvae in soil penetrate skin --> lungs --> trachea --> mucosa of intestines cause vomiting, diarrhea, anemia, can autoinfect
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Strongyloides
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Ingestion of this helminth larvae in pork --> cysticercosis, neurocysticercosis, mass lesions in brain, also found in muscles, skin, heart
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Taenia solium
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eggs in dog feces; hatch in duodenum; can cause cysts in liver, lungs, or bones
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Echinococcus granulosus (hydatid disease)
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nematode from undercooked meat, usually pork; causes inflammation of muscle (coiled larvae encyst in striated muscle), periorbital edema
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trichinella spiralis
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snails are host of this parasite, cercariae penetrate skin, cause granulomas, fibrosis, inflammation of spleen and liver
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Schistosoma
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nematode transmitted by mosquito, causes blockage of lymphatic vessels --> fibrosis, hyperkeratosis (elephantiasis)
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Wuchereria bancrofti (lymphatic filariasis)
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nematode transmitted by black flies; causes hyperpigmented, chronically itchy skin and "river blindness"
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Onchocerca volvulus
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Chlamydiae, Mycoplasmas, Rickettsiae
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100-1000nm Obligate intracellular parasite Similar to bacteria but lack essential characteristics. Chlamydia lack ATP synthesis. Mycoplasmas lack a cell wall.
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Structure of gram negative
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2 lipid bilayers with sandwiched peptidoglycan layer, covered by a cell wall
Escherichia coli (anaerobic) Klebsiella (anaerobic) Enterobacter (anaerobic) Proteus (anaerobic) Serratia Pseudomonas Bacteroides (anaerobic) Shigella (facultative anaerobe) Salmonella Yersinia Cholera |
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Structure of gram positive
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Gram postive – single bilayer covered with peptidoglycan and a cell wall
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Structure of funghi
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2-200um Thick ergosterol cell walls
Candida |
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What are protozoa?
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1-50um Single celled organisms with motility, pliable plasma membranes, complex cytoplasmic organelles.
Giardia |
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What are helmlinths?
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Highly differentiated multicellular organisms with complex life cycles. Roundworms – nematodes (ascaris, hookworms, strongyloides, trichinella)
Flatworms – cestodes (tapeworms, cysticerci, hydatid cysts) Flukes – trematodes (schistosomes) |
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What are ectoparasites?
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Arthropods – lice, ticks, fleas
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Give examples of how organisms evade barrier methods of immunity?
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Gram-negative organisms have fimbriae or pili that mediate adherance to specific cells of the host
Gram-positive organisms have fibrillae that bind to the surface of all eukaryotic cells Respiratory viruses can attached to surface carbohydrates and evade mucociliary clearance. Some respiratory viruses can degrade mucus. Haemophilius and bordetella make toxins that paralyse cilia. |
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How do some organisms hide from the immune system?
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Gallbladder, lumen of the intestine, keratinised epithelium
-Salmonella Intracellular evasion - rapid entry of pathogen into cells offers protection -Malaria |
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How do pathological organisms modify the immune system to avoid being killed?
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Resisting phagocytosis.
Mycobacterium TB is resistant to phagocytosis. Pseudomonas secretes a leukotoxin that kills neutrophils. Immune evasion by varying or shedding antigens: Pneumococci capable of 80 variations of their capsular polysaccharides. Neisseria and borrelia can vary their surface antigens Infection of cells of the immune system: HIV and EBV directly infect cells of the immune system and reduce immune response Inhibition of complement: Staphylococci are covered by protein A molecules which bind Fc and therefore inhibit phagocytosis Some E coli prevent complement activation Some gram negative bacteria have long polysaccharide chains which activate complement away from the cell membrane. Inhibition of cytokines:-HBV Suppression of MHC1-Adenovirus Inhibition of B cell activation-EBV Inhibition of antibody- Neisseria, haemophilius, streptococcus secrete proteases that degrade antibodies. |
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Difference between endotoxin and exotoxin?
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Endotoxin – lipopolysaccharide that is a structural component of the outer cell wall of gram negative bacteria.
Exotoxin – enzymes (coagulases, fibrinolysins etc.) that act on a substrate – eg diphtheria toxin |
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Structure and epidemiology of haemophilus influenzae
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Pleomorphic, gram- negative organism
Encapsulated and unencapsulated forms Type B (encapsulated) causes most severe disease |
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Morphology of TB?
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Aerobic non-spore forming, non motile bacilli with a waxy coat which retains red dye in acid fast stains.
Droplet spread |
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Effects of TB?
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Evasion of phagocytosis by macrophages by production or cord factor and LAM that inhibit macrophage activation
Induction of delayed type IV hypersensitivity by secretion of heat shock proteins Induction of macrophages to secrete TNF resulting in fever, weight loss and tissue damage Inhibition of T cell proliferation by secretion of IL10 |
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Pathology of TB
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Inhalation of mycobacteria. Phagocytosed by macrophages but not lysed. Transported to hilar lymph nodes.
Mycobacterium multiplies and is phagocytosed by further macrophages – dissemination may occur. Delayed type IV hypersensitivity is demonstrated by CD4 T cell secrete gamma interferon which activate macrophages to kill mycobacteria via activated nitrogen intermediates CD8 T cells cause mycobacteria lysis T cells (CD4 and CD8 negative) lyse macrophages without killing mycobacteria. These mechanism result in the formation of a granuloma (subpleural, usually just above or below interlobar fissure) and eventually to the formation of calcified scar in lung parenchyma and hilum – ghon complex. |
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Describe the pathology of secondary TB?
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May occur due to reinfection, reactivation or direct progression of primary disease. Multiple granulomas form – most commonly in apex of lung, also in kidneys, meninges, other organs.
Miliary TB represents massive haematogenous spread. Caseous necrosis and cavities may form and therefore produces more damage than does primary TB. |
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Structure of rotavirus?
Pathogenesis of rotavirus? |
Encapsulated DS-RNA genome.
Faecal-oral transmission Invades and destroy mature epithelial cells in the middle and upper villus. Diarrhoea caused by reduced absorption of sodium and water from the lumen. |
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Campylobacter
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Most common cause of bacterial gastroenteritis
Campylobacter jejuni. Flagellated gram negative. Faecal-oral transmission. Associated with ingestion of chicken. Flagellae necessary for penetration of mucus. Invades epithelial cell. Associated with reactive arthritis in HLA B27 individuals Also associated with Guillain Barre syndrome |
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What organisms cause shigella dysintery and what are their properties
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Shigella dysenteriae, flexneri, boydii, soneii.
Gram negative facultative anaerobe. aecal-oral transmission. Tiny number of organisms required. Invades intestinal mucosa but does not go beyond the lamina propria. Bacteria multiply and causes cell death. Shiga toxin causes haemorrhagic colitis, HUS and Reiter’s syndrome. Associated with reactive arthritis in HLA B27 individuals Mucosa becomes hyperaemic and oedematous. Enlargement of lymphoid follicles. Fibrinosuppurative exudate forms a pseudomembrane. Mucosa becomes soft and friable with superficial ulceration. |
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Amoebiasis?
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Common in developing countries
Cysts are resistant to gastric acid. In the colon, cysts release trophozoites that then reproduce. Trophozoites attach to and invade colon wall to cause dysentery. |
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Giardiasis
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Most prevalent intestinal protozoan worldwide.
Cysts resistant to chlorine in water supplies. Faecal-oral transmission. 2 forms – trophozoites and cysts. Trophozoites multiply in duodenum and adhere to epithelial cells but do not invade. Trophozoites form cysts again as they move away from cholesterol rich areas in the duodenum. Trophozoites are pear shaped and binucleate. Cause clubbing of villi nfection often subclinical. Causes variable acute, chronic diarrhoea, steatorrhoea, constipation |
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HSV under the microscope?
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HSV typically forms Cowdry inclusions – pink/purple virions that push host cell chromatin to the edge of the cell.
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Chicken pox and shingles clinical?
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Chicken pox Initial respiratory type illness. Rash appears after 2 weeks Rash is typically vesicular Vesicles crust and resolve
Shingles Involve sensory nerves of one or more dermatomes May cause facial nerve paralysis due to the Ramsey Hunt syndrome Complications Interstitial pneumonia Encephalitis Transverse myelitis |
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EBV morphology?
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Lymphocytosis with atypical lymphocytes. Enlargement of lymph nodes and spleen.
Infectious mononucleosis – benign self limiting lymphoproliferative disease characterised by fever, generalized lyphadenopathy, splenomegaly and sore throat. Rarely progresses to hepatitis, menoingoencephalitis, pneumonitis. |
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Legionella
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Legionella pneumophila
Facultative intracellular parasite of macrophages Droplet spread Resistant to cooling Associated with cooling and air conditioning systems Bacteria are phagocytosed by macrophages then inhibit oxidative burst and phagosomal fusion Infection tends to affect peripheral respiratory tract and spare bronchi and proximal bronchioles Small abscesses are common Healthy individuals usually develop self limiting Pontiac fever Smokers, elderly, immunocompromised develop legionnaires disease charcaterised by severe pneumonia |
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Malaria epidemiology?
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Affects 100 million/year.
Kills 1 million/year |
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Types of malaria?
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Plasmodium falciparum
Plasmodium vivax Plasmodium ovale Plasmodium malariae Transmitted by 12 different anopheles mosquito types. |
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Life cycle of malaria parisite?
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Sporozoites transmitted by mosquito bite. Bind to and invade liver cells then multiply.
Hepatocyte ruptures, releasing merozoites into blood. Merozoites bind to and invade red blood cells Some merozoites from gametocytes that infect the next mosquito Most merozoites multiply, resulting in red cell rupture and infection of further red cells The red cell stage is initially called a trophozoite, then a schizont |
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Clinical picture of malaria
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Congestion and enlargement of the spleen – spleen may become fibrotic over time.
Cerebral malaria characterised by vascular plugging with localized haemorrhages and hypoxic changes. Falciparum Fever, severe anaemia, renal failure, pulmonary oedema, cerebral symptoms, death. Cerebral malaria is the cause of 80% of deaths in children Vivax, malariae Mild anaemia, rare splenic rupture and nephritic syndrome |
