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199 Cards in this Set
- Front
- Back
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Endotoxin causes septic shock by causing the realease of___ |
TNF, IL 1, IL 2 |
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3 examples of Host response to infection causing the injuriuos effects. |
HBV damaging liver cells, TB causes tissue damage when TB is attempted to be sequesterd, Post-strep glomerulonephirits from immune complex deposition |
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Measles aka |
Rubeola |
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What class of virus is measles |
RNA paramyxovirus |
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Extremem complications of measles? |
Subacute slerosing panencephalitis, inclusion body encephalitis. |
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Oral lesions of measles called... |
Koplik spots |
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Pathognomonic cells of measles?Where do you find them? |
Warthink-Finkeldey cells--Multinucleated giant cells with eosinophilic nuclear inclusion bodies. In thelymphoid organs, lungs and sputum. |
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How does measles affect the lymphoid organs? |
Follicular hyperlasia, large germinal centers, Warthin-Finkeldey cells |
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Mumps is a ___ virus. |
Paramyxovirus RNA |
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Mumps most often causes enlarged ___ |
Parotid glands |
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Mumps can infect what organs? |
Parotids, Testes, pancreas, CNS |
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Tissue infected with mumps microscopically would show _________ |
Intersititial edema, diffuse macrophages, lymphocytes and plasmam cell infiltrates. |
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Polio virus is in what family of viruses? |
unencapsulated RNA enterovirus. Other enterods coxsackievirus, echovirus, hep A. |
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What part of nervous system can polio invade? |
Motor neurons or brain stem (leads to bulbar poliomyelitis--->resp paralysis) |
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WNV is what class of virus? |
Arbovirus (arthopod-borne) of the flavivirus (includes dengue and yellow fevers, eastern encephalitis). |
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Symptoms of WNV? |
Acute falccid paralysis due to meningitis, encephalitis, meningoencephalitis). Indistinguishable fomr polio. Rarely hepatitis, myocarditis, pancreatitis. |
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Who's at greatest risk for WNV? |
Elderly and immunosuppressed. |
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Viruses that cause Viral Hemorrhagic fever? |
BAFF - Bunyaviruses, Areanaviruses, Filoviruses, flaviviruses |
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Most viral hemorrhagic fevers infect _________. What causes the hemorrhaging? |
Endothelial cells. Bleeding causes by endothelial dysfunction, platelet dysfunction or thrombocytopenia. |
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Herpes viruses are what type? |
DS DNA |
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HSV-1 leads to _________. |
Cold sores, gingivostomatitis, corneal blindness |
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HSV-2 leads ______. |
Genital warts |
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Leading causes of corneal blindness? |
HSV-1 infections |
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Worst cases scenario in HSV infections |
Disseminated viseral infections and encephalitis. |
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Life cycle of HSV? |
Replicates in infected skin or membrane, resides latently in neurons, spreads from ganglia back to skin or MM. |
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Microscopic appearance of HSV infection? |
Cowdry-type A inclusions--Virion inclusions cause chromatin to be compressed against nuclear membrane. Tzanck prep shows multinucleated syncytia. |
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In most cases, CMV is ______. |
Asymptomatic nearly always except in neonatesa nd immunosuprressed. |
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Most common pathogen infected AIDS victims? |
CMV - life threatening |
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Histologic appearance of CMV infection? |
Cellular enlargement, purple intranuclear inclusions with clear halo, small basophilic cytoplasmic inclusions |
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Where does VZV lay dormant? |
In sensory dorsal root ganglia. |
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Histologic appearance of VZV? |
Vesicles contain epithelial cell intranuclear inclusions. Blisters appear identical to HSV (Intranuclear inclusions compressing chromatin against nuclear membrane). |
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Why is Hep B so hard to remove from the body? |
High mutation due to it's DNA denome being transcribed by an RNA template (no proofreading) |
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How does Hep B damage liver cells? |
HBV infects hepatocytes but the immune reponses causes the damgage. |
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What determines if a person is a Hep B carrier or not? |
cytotoxic T cell response can clear it. |
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Hep B puts one at risk for _______ |
Hepatocellular carcinoma, cirrhosis and esp. chronic hepatitis. |
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3 viruses implicated in causing human cancer? |
EBV, HPV, HTLV-1 |
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EBV infection symptoms? |
fever, sore throat, generalized lymphadenopathy, splenomegaly, very high WBC count. |
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Life cycle of HBV? |
Infects nasopharyngeal or ooparyngeal epitheliaium, progressing to B cells--the reservior. T cells proliferate kill the infected B cells. |
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HBV infections demonstrate what special cells in lymph nodes? |
Reed-Sternberg-like cells (large binucleate cells). |
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EBV + immunocompromised can lead to _______. |
B-cell lymphoma. |
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EBV can lead to what 2 types of cancer? |
B-cell lymphoma and Burkitt's lymphoma. |
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Mutation in EBV associated Burkitt's lymphoma? |
8:14 translocation on the c-myc oncogene into the Ig heavy chain region. |
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HPV causes what process in ipithelial cells? |
Koilocytosis--vacuolizatoin of epithelial cells. |
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How does HPV promote unwanted cell growth? |
E6 and E7 dysregulate the cell cycle. |
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Staph aureus virulence factors? |
Surface proteins (adherance), enzymes that degrade host proteins, hemolysins (kill cell membranes), exfoliateive toxins, enterotoxins, superantigens. |
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characteristic Staph aureus inflammation? |
Pyogenic local destructive inflammation. |
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Staph that infects catheterized, prosthetic heart valve, or IV drug users? |
Staph epidermidis |
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Staph that causes UTI? |
Staph saprophyticus. |
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All the things strep A (pyogenes) can cause? |
Pharyngitis, scarlet fever, erysipelas, impetigo, rheumatic fever, TSS, necrotizing fascitis, glomerulonephritis. |
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95% of people infected with CMV are ________. |
Asymptomatic |
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CMV infections in infants produces what disease? CMV in immunocompromised produces what disease? |
Cytomegalic inclusion disease. Disseminated CMV (life threatening) |
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Features of Cytomegalic inclusion disease (in infants)? |
Hemolytic anemia, jaundice, hepatosplenomegaly, pneumonitis, deafness, chorioretinitis, brain damaged, Thrombocytopenia. |
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Features of disseminated CMV infection? |
Life threatening. Lung, GI, retina primarily involved. focal necrosis and little inflammation. |
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Histologic CMV? |
Cellular enlargemnt, large purple intranuclear inclusions surrounded by clear halo with small basophilic cytoplasmic inclusions. |
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How is VZV transmitted and how does it spread? |
Aerosols; hematogenously to trunk then head and extremities. |
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Histology of vesicles and blisters of VZV? |
Vesicles have epithelial cell intranuclear inclusions; blisters are identical to HSV. |
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Where does Herpes zoster (shingles) come from? |
VZV latent in DRG infecting sensory nerves. |
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HBV is what kind of virus? Causes chronic or acute hepatitis? |
DNA of hepadnavirus family. Causes both acute and chronic |
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How is HBV transmitted? |
Percutaneously, perinatally and sexually. |
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Why does HBV stay in the blood for so long? |
Lots of mutations due to it being synthesized by reverse transcription of RNA template (no proof reading). |
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How does HBV damage the liver? |
Immune response kills liver, the virus does not. |
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What determines if a person is a carrier of HBV or not? |
cytotoxic T-cell immune response. |
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Histology of chronic HBV infection? |
Lymphocytic infalmmatino, hepatocytic apoptosis; can lead to cirrhosis and increased risk for hepatocellular carcinoma. |
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Three viruses that cause cancer? |
EBV, HPV, HTLV-1 |
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Infectious mononucleosis symptoms. |
fever, sore throat, generalized lymphadenopathy, hepatosplenomegaly, and VERY high WBC count. |
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Progression of EBV virus infection? |
Begins in naso/oropharygeal epithelial cells, infects B cells (the reserivoir), T-cells kill the infected B cells. |
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Histology of lymph nodes in EBV infection? |
Increased T cells and Reed-Sternburg-like cells (large binucleate cells). |
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EBV can lead to what cancers? |
B-cell lymphoma (in immunocompromised), Burkitt's lymphoma (8:14 translocation on c-myc of heavy chain) |
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Histology of HPV? |
Koilocytosis- Perinuclear vacuolization of epithelial cells. |
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Mechanisms of HPV's promotion of cell growth? |
E6 and E7 dysregulate the cell cycle. |
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Staph aureus virulence factors? |
Adhesion proteins, enzymes that degrade host proteins; toxins: hemolysisns (damage membranes), exfoliative toxins, enterotoxins, superantigens. |
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Which staph attacks those with prostetic heart valves and IV drug users? |
Staph epidermidis. |
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Which staph frequently causes UTIs? |
Staph saprophyticus |
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Two beta hemolytic streps? |
Pyogenes (A), agalactiae (B) |
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Strep pyogenes can cause... |
pharyngitis, scarlet fever, erysipelas, impetigo, rheumatic fever, TSS, necrotizing fascitis, glomerulonephritis. |
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Strep agalactiae colonizes where? |
The vag. |
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Strep agalactiae can cause ____ |
Chorioamnionitis in pregnancy and neonatal sepis and meningitis in neonates. |
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Alpha hemolytic strep includes... |
Strep pneumoniae, Viridians (including s. mutans). |
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Strep. pneumoniae can cause... |
Adult community-acquired pneumonia and meningitis. |
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Strep viridians can cause...where do you find strep viridians? |
Dental caries (S. mutans) and endocarditis.Normal flora of the mouth. |
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enterocci can cause... |
endocarditis and UTIs. |
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Strep virulence factors? |
Capsule (group A), M-proteins inhibit the alternate pathway of completment activation (S. pyogenes), pneumolysis destroy membrane and damage tissue (S. pneumonia) |
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Lifecycle of C. diphtheriae? What organs does it affect? |
Colonizes oropharynx and fires off exotoxins to damage the heart, nerves and other organs. |
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Virulence factors of C. diphtheriae and what they do? |
B fragment facilitates entry of A subunit. A subunit blocks protein synthesis via ADP ribosylation. |
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Listeria Monocytogenes is gram pos or neg? |
Pos. |
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Who does Listeria infect? |
Elderly , immunosuppressed, pregnant women and their fetus. |
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What causes granulomatosis infantiseptica? |
Listeria Monocytogenes infecting a fetus. |
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What does listeria cause? |
Meningitis and sepis in elderly, immunocompromised and pregnant ladies. |
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How does listeria infect cells? |
Binds E-cadherin to stimulate phagocytosis, then uses listeriolysin O and phospholipases to excape phagosome and cytoplasm. Then ActA propels the bacteria into adjacent cells. |
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three classes of B. anthracis infection. |
cutaneous, Inhalational, Gastrointestinal. |
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Signs of cutaneous antrhax infection. |
Painless, pruritic papules leading to vesicles and then to black eschar. |
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Signs of resp. antrhax infection. |
Rapid sepsis, shock, death. |
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Signs of GI antrhax infection. |
Severe blood diarrhea and often death. |
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Anthrax toxins and how they induce damage. |
Edema factor - converts ATP to cAMP leading to cellular water efflux. Lethal factor- protease that estroyes MAP kinase kinase, killing cells |
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Histology of anthrax-infected cells? |
Necrois, neurto and macrophages, and large rectangular extracellular bacteria chains. |
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Nocardia is what kind of bacteria? |
Aerobic Gram-positive in branches. (also stains with modified acid fast stains-Fite-Faraco stain) |
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Nocardia asteroides causes what? |
Opportunistic indolent resp infections, often with CNS infection. |
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Histology of Nocardia asteroides infected cells. |
Granulation tissue and fibrosis. branching and can be stain with modified acid-fast (Fite-Faraco stain). |
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Neisseria are what kind of bacteria? |
Aerobic, gram neg, dipococci |
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N. Meningitidis affects which age group? |
5-19 year olds, esp in those w/ terminal complement deficiencies. |
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N. Gonorrhoeae symptoms in males, females, and neonates? |
Males- UrethritisFemales- usu. asymptomatic; can lead to PID, infertility and ectopic pregnancy.Neonates- Blindness and rare sepsis. |
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How do Neisseria evade immune responses? |
Expression of alternative genes for adhesive pili and OPA proteins. |
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Symptoms of Bordetella pertussis? |
Paroxysm coughs, laryngotracheobronchitis, mucosal erosions, mucopurulent exudate, lymphocytosis. |
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Pseudomonas aeruginosa usually affects what 3 groups of people? |
CF, burn victims, neutropenia. |
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In CF patients, how does pseudomonas aeruginosa evade immune responses? |
It secretes exopolysaccharide (alginate) forming a protective biofilm. |
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What can Pseudomonas aeruginosa do to neutropenics? |
Tissue necrosis via vascular invasion and thrombosis. |
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What causes plague? |
Yersinia pestis. |
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what causes iletis and mesenteric lymphadenitis? |
Yersinia enterocolitica and yersinia pseudotuberculosis. |
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symptoms of the plague? |
Lymph node enlargement (buboes), pneumonia, sepsis, tissue necrosis, neutrophilic infiltrate. |
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What causes chancroid (soft chancre)? Symptoms? |
Hemophilus ducreyi. Ulcerative genital infection. |
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How do you get Granuloma inguinale? |
STD caused by calymmatobacterium donovani. |
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How does granuloma inguinale progress? |
Starts as a papule on genitalia (or mouth/pharynx) then ulcerates and granulates into SOFT PAINLESS mass. Can cause urethral, vulvar or anal strictures. |
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Histology of Granuloma inguinale? |
Pithelial hyperplasia at ulcer borders with neutrophils. |
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What cells do M. tuberculosis infect? |
Macrophages that should be kill by T-cells 2-4 weeks later. |
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First exposure to TB causes what? |
95% asymptomatic, 5% have lobara consolidation, hilar adenopathy and pleural effusion; rarely spreads via lymph-->miliary. |
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Symptoms of secondary TB (after latent TB is reactivated)? |
Cavitation in apex of upper luns, low fever, night sweats, weight loss. |
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Appearance of primary and secondary TB? |
Primary- Lung and LN granulomas called Ghon complexes.Secondary-Circumscribed focus of caseation can heal with fibrosis. |
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What population and where in the body do you find Mycobacterium avium-intracellulare complex? |
Immunocompromised folks; widley disseminated throughout the body. |
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What organism causes leprosy? |
Mycobacterium leprae. |
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How does leprosy spread throughout the body? |
Spreads via the blood after being phaged by monocytes or alveolar macrophages. |
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Two types of leprosy and symptoms? |
Tuberculoid- insidious dry scaly skin lesions w/o sensation, peripheral nerve involvemnet.Lepromatous- Disfiguring,Perineural macrophage and Schwann cell invasion. |
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What determines if a leprosy infection will be tuberculoid or lepromatous? |
Tuberculoid- T-helper 1 response (TNF-gamma)Lepromatous- ineffective T-helper 2 response. |
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Name the spirochetes. |
Syphilis (treponema pallidum), Borrelia recurrentis (relapsing fever), Lyme (Borrelia burgdorferi) |
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Primary syphilis symptoms. |
3 weeks after sexual contact, firm painless raised lesion (CHANCRE) at infection site. Self-healing. Lesion demonstrates endarteritis. |
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who gets secondary syphilis? |
75% of those who don't treat their primary syph. |
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secondary syphilis symptoms? |
Mucocutaneous lesions, lymphadenopathy, fever, malaise, weight loss. |
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Who gets tertiary syphilis? |
1/3 of untreated infected pts. >5 years later. |
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Tertiary syphilis symptoms? |
CV syphilis- aortitis (endarteritis of vasa vasorum), aortic root dilation, aneurysm, and aortic valve insufficiency.Neurosyphilis- meningovascular disease, tabes dorsalis, brain parenchymal disease, or protein, WBCs, low glucose in CSF. |
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When do you see gummas? |
In benign tertiary syphilis. |
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congenital syphilis symptoms? |
Death 25%, nasal discharge, skin sloughing, hepatomegaly, skeletal abnorms. Later- notched incisors, deafness, blindness (Hutchinsons triad). |
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How is replapsing fever transmitted? |
Louse transmit Borrelia recurrentis (epidemic). Ticks transmit other types of borrelia (endemic). |
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What causes the relapses in replapsing fever? |
Variation of the surface proteins of Borrelia |
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Symptoms of relapsing fever/ |
Chills, fever, HA, DIC, multiorgan failure. |
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Lyme dz cause by and transmitted by... |
Borrelia Burgdorferi from ixodes ticks |
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Progression of Lyme dz symptoms. |
1. erythema chronicum migrans (bulls eye), fever, Lymphadenopathy. 2. Hematogenous spread; skin lesions, LNopathy, joint and muscle pain, arrhythmias, meningitis.3. Years later; encephalitis, destructive arthritis. |
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What does the oral anaerobe Fusobacterium necrophorum cause? |
Lemierre syndrome. |
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What's Lemierre syndrome? |
Infection of lateral pharyngeal space with septic jugular vein thrombosis. Caused by Fusobacterium necrophorum. |
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What anaerobe causes Bartholin's cysts abscess and tubo-ovarian abscesses? |
Prevotella species often mixed with E. coli and S. agalactiae. |
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What ususallly causes head and neck abscesses? |
Oral flora--Prevotella, Porphyromonas, mixed with Staph and Strep. |
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What usually causes abdominal abscesses? |
Bacteroides fragilis, Peptostreptococcus, Clostridium, E. coli |
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Clostridium perfringens and C. Septicum cause... |
Cellulitis, muscle necrosis in wounds (GAS GANGRENE), food poisoning, small bowel infection. |
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Histology of gas gangrene? |
Infarct w/o inflammatory cells. |
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How does Clostridium tetani cause tetany? |
Tetanospasmin block GABA, an inhibitory neurotranmitter. |
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How does Clostridium botulinum causes flaccid paralysis? |
Binds to motor neuron gangliosides, and cleaves synaptobrevin, blocking Ach release. |
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What bacteria causes pseudomembranous colitis in antiboiotic-treated pts.? |
Clostridium difficle's cytopathic effects. |
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What causes trachoma? What does it cause? |
Chlamydia trachomatis (serotypes A, B, C). An ocular infection in children. |
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Life cycle of Clamydia trachomatis? |
Elementary body (EB) is the infective particle that transforms into the reticulate body (RB) inside endosomes. |
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Where does C. trachomatis reside in the body. |
In endosommes (an obligate intracellular bacteria). |
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Symptoms of Chlamydia? |
Frequently asymptomatic; epididymitis, prostatitis, PID, pharyngitis, conjunctivitis, perihepatic inflammation, proctitis. |
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What causes lymphogranuloma venereum? |
Chlamydia trachamatis. |
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Symptoms of lymphogranuloma venereum? |
Genital lesions with granulomatous and neutrophils. Caused by C. trachomatis. |
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Three disease Richettsiae cause |
Typhus, spotted fever, ehrlichiosis. |
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What causes epidemic typus? |
Rickettsia prowazekii |
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Typhus symptoms. |
Rash w/ small ehmorrhages to skin ncecrosis and gangrene and internal organ hemorrhages.CNS typhus- nodules w/ microglial proliferation |
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Where do Typhus and spotted fever organisms proliferate? |
Endothelial cells causesing vessel necroisis. |
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Ehrlichiosis results from _____ infecting _____. |
Anaplasma phagocytophila or Ehrlichia ewingii infecting neutrophils, or Ehrlichia chaffeensis infecting macrophages. |
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Symptoms of Ehrlichiosis |
Fever, HA, malaise, resp insufficiency, renal failure, shock. |
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Candida is normally found... |
On skin, mouth, GI. |
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Candida can cause _______ in people with normal immunity. |
Vaginitis (esp. in preganancy), diaper rash, oral thrush. |
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Candida can cause _____ in immunodeficient. |
Mucocutaneous candidiasis (in people with hypoparathyroidism, hypoadrenalism, hypothyroidism.neutropenic pts.- Invasive candidiasis spread hematogenously causing microabscesses. |
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What does Cryptococcus neoformans do to healthy people and the immunosuppressed? |
Healthy - Solitary pulmonary granulomaImmunosuppresed- Small cysts in gray matter of brain, meningoencephalitis in immunosuppresed and pts. w/ lupus, sarcoidosis. |
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Who are the infectious molds? |
Aspergillosis, Zygomycosis (mucomycosis). |
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Aspergillus + peanuts = ? |
Can create AFLATOXIN leading to liver cancer. |
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Pulmonary lesions leftover from TB, bronchiectasis, infarcts, abscesses can be colonized by... |
Aspergillus fumigatus, creating aspergillomas |
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What does aspergillus do to immunosuppresed? |
Necrotizing pneumonia (target lesions), thrombosis; can lead to hemmorrhage and infarction on necrotizing inflammation. |
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Aspergillus + neutropenia = |
sinusitis, pneumonia, Disseminated aspergillus. |
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Asperguillus in previously healthy people leads to... |
An allergic mold. |
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Zygomycosis affects what kind of patients? |
Neutropenic, and ketoacidotic diabetics. |
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What causes zyomycosis? |
Zygomycetes (Mucor, Absidia, Rhizopus, Cunninghamella). Along with neutropenia, ketoacidosis. |
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What do zygomycetes do? |
Can spread from nasal sinues to orbit or brain; can invade arterial walls causing nerosis. |
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What organism causes malaria? |
Anopheles misquitos transmit: Plasmodium falciparum causes the most severe, vivax, ovale, and malariae cause less servere types. |
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How does P. falciparum cause tissue ischemia? |
Infected RBCs adhere to endothelium, creating vascular occlusion. |
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What organs are especially involved in malaria? |
Splenic occlussion and hepatic enlargement (with Kupffer cells), vascular occlusion leads to hemorrhage and ischemia of the brain. |
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Three condition that protect against malaria? |
HbS, Hemoglobin C traits limit malaria proliferation. Some blacks lack the required duffy RBC antigen. |
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How do you get babesiosis? |
Ixodes ticks trasmit Babesia microti. |
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Babesiosis symptoms? |
Fever, hemolytic anemia, esp. in debilitated and splenectomized. |
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What does Babesia microti infect? |
RBCs (thus the hemolytic anemia), creating the tetrads in RBCs. |
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Sandflies transmit.. |
Leishmania species |
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Leishmaniasis symptoms? |
Can be cutaneous or mucocutaneous; mild rashes to disfiguring lesions. |
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Where do leishmanias live in the body? |
in acidic pagolysosomes |
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Tsetse flies transmit.. |
African Trypanosomiasis. |
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Symptoms of Trypanosomiasis? |
Chancres at bite site, fevers, LNopathy, splenomegaly, brain dysfxn (sleeping sickness), cachexia, death. |
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Where do Trypanosomas brucei proliferate? |
In the blood (and in macrophages). |
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Chagas causative agent? |
Trypanosoma Cruzi from triatomids ("kissing bugs"). |
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What activates T. Cruzi? |
acidic phagolysosomes |
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Symptoms of Chagas dz? |
Years after fever, 20% develop cardiomyopathy, arrhythmias, myenteric plexus damage leading to colon and esophageal dilation. |
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Who are the Metazoa? |
Strongyloidiasis, tapeworms, trichinosis, schisto, filariasis, Onchocerciasis. |
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Life cycle of the strongyloidiasis. |
Pentrate the skin, travel in the blood to lungs, ascend trachea, get swallowed, colonize GI, create eggs. |
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symptoms of strongyloidiasis. |
GI symptoms (they invade intestinal mucosa), immunocompromised get disseminated strongyloides. |
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Taenia solium (tape worms) symptoms (pork or human).T. saginata (beef) or Diphyllobothrium latum (fish)? |
Can penetrate the gut wall and disseminate to encyst in brain and other organs.Stay in GI. |
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what causes Hydatid disease? |
Ingestion of echinoccal eggs (Echinococcus granulosus)from dog or fox feces, eggs hatch in duodenum and invade the liver, lungs, and bones forming cysts. |
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How do you get trichinosis? |
Pig and bear meat. |
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symptoms of trichinosis infection? |
Adults spread to muscle causing fever, myalgias, eosinophilia, periorbital edema. Increased gut motility. |
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Histology of trichinosis? |
Membrane-bound vacuoles in myocytes surrounded by eosinophils. |
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How is Schistosomiasis transmitted? Life cycle? |
Freshwater snails; penetrate skin and settle in pelvis or portal venous systems, releasing eggs in stool and urine. |
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Histology of Schistosomiasis? |
Eosinophil-rich granulomas and fibrosis in liver. |
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Causes of Lymphatic filariasis?How is it contracted? |
Wucheria bancrofti (90%), Brugia malayi.Mosquitoes. |
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Black flies transmit... |
Onchocerciasis. |
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Symptoms of Onchocerciasis. Lifecyle? |
Pruritic dermatitis and blindness. Nematodes mate in the dermis producing a nodule (onchocercoma). Eggs accumulate in the skin and eyes. (black fly) |
