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252 Cards in this Set
- Front
- Back
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What are the 3 criteria of an effective immune system?
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1. recognize and destroy a diversity of pathogens
2. recognize and destroy damaged self 3. exhibit self tolerance |
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What happens when the immune system is overactivated?
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autoimmunity and inflammatory diseases
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What happens when the immune system is suppressed?
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immunodeficiency
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What are the clinical aspects of tolerance?
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failure to resolve inflammation
autoimmunity allergy transplant rejection pregnancy anti-tumor responses |
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What are the two types of tolerance?
Which type of tolerance is AIRE? What is the main active mechanism of tolerance? What modulates these mechanisms? |
central and peripheral
central suppressor cells hormones and neural |
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What are the sites of immune privledge?
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brain, eye, gonads, pregnant uterus
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What is central tolerance?
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clonal deletion of highly self-specific T cells.
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What is passive peripheral tolerance?
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in lymph and spleen, exposure to antigens without danger signals induces anergy or death
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In costimulation, what molecule from APc interacts with CD28 from T cells?
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B7
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How does CTL-4A shut down T cell activation?
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T cells expressive CTLA-4 which prevents CD28 binding to B7. After binding to B7, it dephosphorylates CD3 shuting down the TCR dependent signaling pathways.
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Through what interaction can T cells license additional APCs?
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CD40-CD40L
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What handles inhibitory interaction of T cells affecting APCs?
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Tregs
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What are the two sources of CTLA-4? What kind of APCs cause creation of Tregs?
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induced by activation of CD4T and constitutively expressed by Tregs
tolerogenic |
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What are the cytokines secreted by Tregs? What else secretes these?
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IL-40, TGFBeta
viruses |
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What do TGFbeta and IL-10 do?
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suppress T cell activation
act on APCs to cause induction of Treg pehnotype in CD4 T cells |
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What is the initial effect of TGFbeta?
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pro-inflammatory
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Does TGFbeta affect regulatory phenotype in peripheral or central Tregs?
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peripheral
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What is T cells differetiation influenced by?
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DC, immune sensing, and local cytokines
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What can overcome Tregs?
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strongly activated T cells
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What is the mucosa an interior extension of?
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The skin
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What are the goals of the gut, respiratory, and urogenital regions?
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Gut: breakdown of food; absorption of nutrients
Respiratory: exchange of oxygen and CO2 Urogenital: viability and motility of gametes |
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Why do most pathogens enter the body
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mucosa
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What is a major reason pathogens come through the mucosa?
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Large surface area, not as well protected as skin
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What is the leading cause of death among mucosal infections?
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Acute respiratory infections
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What are the 4 regions of Mucus Associated Lymphoid Tissue?
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Nasal, Bronchial, Gut, and Reproductive (Urogenital)
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What are pathogens associated with nalt and balt, galt, and ralt?
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NALT and BALT: Influenza, Pneumonia GALT: Salmonella, Shigella, Polio RALT: Chlamydia, HIV, Gonorrhea
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How is the immune response different for the MALT compared to systemic?
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there are separate inductive (peyer's patch) and effector (lamina propia) lymphoid sites.
most of the antibody-producing cells and effector T cells are found throughout MALT. (not just at the site of an infection) a chronic adaptive immune response is sustained in the intestinal mucosa. – designed to promote tolerance has TGFbeta and IL-10 to dampen response major antibody isotype in mucosal secretions is secretory, dimeric IgA.- doesn’t activate complement or engage NK cells. Non-inflammatory d effector T cells exist within MALT there are separate inductive and effector lymphoid sites |
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What are the NALT, BALT, GALT, and RALT secondary lymphoid tissue?
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Waldeyer's Ring, bronchus associated lymphoid tissue, lamina propia and Peyer's Patch, and urogenital lymphoid tissue.
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What is the purpose of GALT epithelial cells?
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GI function is absorption of nutrients
Respond to PAMP’s and secrete cytokines Transport IgA into lumen |
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What is the purpose of goblet cells?
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Secrete mucus, reduces bacterial access
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Where are Paneth cells found?
What are their purpose? |
bottom of crypts
Release β-defensins (antimicrobial peptides) |
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Where does lymph drain into in MALT?
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lymphoid follicles
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What is a cluster of follicles in MALT?
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Peyer's Patch
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What are the sections of GALT?
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follicle, germinal center, T cell area, dome, and epithelial (M cells)
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What are microfold cells? What do they do?
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Microfold (M) cells of the follicle associated epithelium.
Take antigen from lumen and give to APC DCs. |
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Besides M cells, what are 3 what are antigen to get sampled?
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DCs also sample the lumen for antigens (2).
Antigen can also be transported by epithelial cells (3) or can pass through tight junctions between epithelial cells (4) |
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In GALT, where do DCs present antigen?
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Peyer's Patch or mesenteric lymph nodes
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What secretes different cytokines that determine isotype switching?
What acts as a critical molecular switch in B cell conversion to IgA producing plasma cells? |
effector helper T cells
TGF-β |
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Where do effector lymphocytes from the systemic circulation home?
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to the lamina propria of the GI tract (and possibly other mucosal sites).
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How does IgA get across mucosal epithelial cells?
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poly-Ig receptor
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What properties of IgA make it good for the GI?
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resistant to proteolysis
poor activator of complement inhibits: bacterial adhesion, macromolecuel absorption, inflammation neutralizes virii and toxins |
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What is “Common Mucosal Immune System”?
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The generation of effector lymphocytes in the circulation their subsequent homing to all mucosal sites
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What sites are protected by oral vaccines and what sites are protected by nasal vaccines?
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Intestine, nipples, face
lungs, urogenital, face |
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How is human gut flora controlled?
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saliva, stomach acid, bile, epithelial barrier, water and electrolyte secretion, mucus, antimicrobial products, IgA.
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Match the following 9 terms into 3 triplets:
food, gut flora, pathogens tolerance, mucosal immunity, systemic immunity suppression and lack of response, gut homeostasis, inflammation |
food-tolerance-suppression and lack of response
gut flora-mucosal immunity- gut homeostasis pathogens- systemic immunity- inflammation |
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How do oral and nasal antigens affect skin response? What is the caveat?
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Oral Tolerance prevents TH1 response to skin antigen
IgA response still occurs |
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Describe celiac disease.
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Gluten in wheat degraded into antigenic peptides that trigger immune responses, diarrhea and consequent malnutrition
Associated with HLA class II DQ2 Anti-tissue transglutaminase (TTG) IgA antibodies diagnostic |
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How do you diagnose celiac disease?
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Duodenal biopsy-villous atrophy
However villous atrophy can be also observed as a result of: Infection (Giardia, M.Tb, HIV) Chronic inflammation (Crohn’s, intestinal lymphoma, other dietary foods) Other autoimmune conditions Thus, these need to be considered in differential diagnosis Serologic testing is the diagnostic standard -IgA antibodies against gliadin, connective tissue (recticulin, endomysia), and tissue transglutaminase. -antibody titers correlate with degree of mucosal damage Absence of HLA-DQ2 or HLA-DQ8 has a high negative predictive value |
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What do patients with celiac disease have a higher chance of developing?
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cancer
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What do gut pathogens break in order to gnerate inflammation?
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tolerance
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What does the gut secrete and suppress to generate tolerance?
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TGFB, IL-10
IFN-gamma, IL-12 |
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Which has larger surface area, intestine or skin?
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Intestine
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What are the ways the mouth is protected against pathogens?
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Sloughing Cells
Flow of Saliva Lysozyme sIgA Resident Microflora Lactoferrin |
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What are the ways the stomach and small intestine are protected against pathogens?
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Low pH
Proteolytic Enzymes Fast Flow Mucus, Sloughing Cells Bile, sIgA, Defensins |
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How is the colon less protected than small intestine? How is it better protected?
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Slow Flow,
Mucus, Sloughing Cells, Abundant Microflora |
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What are bacteria useful for?
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Nutrition
Protection from pathogens |
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What the resident microflora in stomach, small intestine, and colon?
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stomach- helicobacter, few if any
duodenum and ileum- relatively few ileum- Numbers rise-like colon, but more facultative colon- Mainly Anaerobes Bacteroides (Gm-) ~30% Firmicutes (Gm+) ~30% Clostridium; Eubacterium Lactobacilli Actinobacteria (Gm+) Bifidobacterium Proteobacteria (Gm-) Facultative enterics (<0.1%) E. coli; Klebsiella |
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How much of nutrients come from bacterial digestion?
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10% of nutrients
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What can decrease microflora and increase chance of infection?
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Malnutrition
Decreased stomach acid Decreased flow rate Decreased turnover of epithelial cells Cancer Chemotherapy Blocks turnover of epithelial cells Kills normal flora Antibiotics Kills normal flora Proton Pump Inhibitors Decreased stomach acid |
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What are the 3 causes of diarrhea?
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Secretory
Inflammatory Malabsorptive |
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What is dysentery?
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Damage to the mucosa
Blood and mucus in stool |
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What is Gastroenteritis?
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Pain associated with inflammation of lamina propria or mesenteric lymph nodes
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What is a consequence of GI tract infection?
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Toxin Production or Reactive Arthritis
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What does an absence of Tregs cause? What does a mutation in Fox3P cause?
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autoimmunity
IPEX |
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What disease can be treated with Tregs?
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Glucocorticoid treatment for asthma increases Tregs
Anti-TNFa for Crohn’s disease increases Tregs (Ricciardelli 08) |
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What is Salmonella typhimurium?
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salmonella in mice that is well studied
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What are the symptoms of normal salmonella? What are the treatments?
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Acute enteritis, abdominal pain, diarrhea, nausea, headache, and fever. Reactive arthritis. Aortic aneurysms.
Treatment Rehydration Antibiotics in systemic cases. |
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How does salmonella invade intestinal epithelium?
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Pili for Colonization
SPI-1 Type III Secretion System |
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How is SP-1 regulated?
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SPI-1 is exquisitely regulated by the environment
Oxygen, Osmolarity, pH, Bile Specifically turned on in the intestine Numerous Regulatory Proteins Feed into the System |
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What are some SP-1 proteins?
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~10 Effector Proteins are Injected
SopE Induces cytoskeletal rearrangement and inflammation Guanine Exchange Factor (GEF) for Rac1 SptP Dampens response to allow cell to regain normal architecture GTPase Activating Protein (GAP) for Rac1 SipA Lowers critical concentration actin require for polymerization |
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What is the effect of Rac-1?
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membrane ruffling, inflammation, and Nk-kB activation
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What does the SipA protein, an SPI effector protein, do?
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faciliates actin rearrangement
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Why does Salmonella Typhi not normally cause diarrhea?
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Capsule (Vi) blocks IL-8 production
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What is the normal autopsy hallmark of typhoid infection? What is the complication of typhoid? Why do we need hand washing?
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Invades and causes ulceration of Peyer’s patched
Systemic infection Carrier State |
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What are the effect of SPI1 effectors?
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Invasion
Inflammatory Diarrhea PMNs in stool ~10% of patients have blood in stool Macrophage Necrosis SipB Caspase 1 (ICE) Induces Necrosis and inflammation Propagation in Peyer’s patches Caspase-1 KO mice are resistant to Salmonella |
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How can Salmonella mutants defective in both pili and the SPI1 T3SS still gain access to systemic sites? Hint: what is SPI1 independent invasion?
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Dendritic cells reach out and grab the bugs
In the case of Salmonella, this is not a good idea |
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What will prevent tymphimurium infection? What is the complication
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IgA directed against Typhimurium O-antigen will prevent infection
Functional at the same concentration required to agglutinate Problem: there are >2000 serotypes of non-typhoidal Salmonella |
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How does salmonella cause inflammatory diarrhea? Is inflammation good or bad? How does S. typhi block inflammatory response?
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Salmonella interaction with epithelial cells initiates inflammatory diarrhea
SPI1 injection induces IL-8 Flagella and LPS induces IL-8 and TNF PMN infiltration Increasing evidence suggests that inflammation facilitates growth of Enterobacteriaceae S. typhi specifically blocks the inflammatory response via the capsule |
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Where does salmonella infection start and end?
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Bacteria spread from the Peyer’s patches to systemic tissue
Initially spleen, liver, and bone marrow Ultimately all tissues |
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Where does systemic salmonella primarily grow? What factors enable it?
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Bacteria are primarily replicating in macrophages
PhoPQ regulon SPI2 T3SS |
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How does systemic salmonella spread?
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Macrophages apparently lyse and bacteria are taken up by new macrophages
Uptake is via opsonization NOT bacterial mediated invasion |
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What does SPI-2 do?
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Basically enables salmonella to grow in macrophages
Redirects the normal phagolysosome maturation Forms “Salmonella Containing Vacuole” SPI-2 is induced intracellularly Effector proteins alter vesicular trafficking |
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What do you do for Typhi and Paratyphi?
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Antibiotics (Cipro) for systemic cases and certainly in Typhi and Paratyphi
Oral rehydration |
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How do you diagnose salmonella?
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Plate stool sample on Lactose MacConkey or Salmonella-Shigella selective medium
Lac- Biochemical confirmation Enterotube: H2S production et al. Serological identification |
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What does PhoPQ do?
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PhoPQ contorls transcription of virulence factors
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What bacteria is the basis for MRSA and is normally found in the nose?
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Staphylococcus aureus
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What are the toxins of Staphylococcus Aureus?
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Produces about 8 types
Hemolysins Leukocidin (kills phagocytes) Superantigens Toxic Shock Syndrome Toxin - 1 Enterotoxins Others |
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How does food become infected with Staphylococcus aureus? Does cooking help?
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Snot
No |
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What are the symptoms and mechanisms of staphylococcal food poisoning?
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Toxinosis
Bacterial cells are irrelevant although can be isolated from stool and vomitus Symptoms have rapid onset (6-12 hours) and rapid resolution (12-24 hours) Projectile vomiting and diarrhea Mechanism is not clear Directly affects “vomiting center” of brain - emetic Superantigen and emetic effects are genetically separable Treatment – oral rehydration |
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Where do you find clostridium? What are the 3 most famous strains?
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soil
Clostridium botulinum - botulism Clostridium tetani – tetanus Clostridium perfringens – gas gangrene and food poisoning |
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Which toxin is heat labile?
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botulism
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How does Botox work? What does it helpwith?
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Proteases that cleave various “SNARE” proteins at neuromuscular junctions
Blocks acetylcholine release Flaccid paralysis Neurotransmitter blockage is irreversible New terminals can “sprout” in 2-3 months “Botox” (commercially available serotype A) is used to treat a variety of “overactive muscle” disorders Dystonias, ocular motility, spacticity, and more recently cosmetic applications |
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What causes infant botulism?
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Honey and lack of microflora
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What are the symptoms of botulism?
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Food-mediated
Difficulty in focusing vision, swallowing, and other cranial nerve functions Progressive striated muscle paralysis 15% fatality from respiratory failure Symptoms start 12-36 hours after ingestion No fever or sepsis Reportable |
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What is the treatment for botulism?
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Treatment
Antitoxin (horse serum) from CDC Supportive therapy |
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Describe Clostridium perfringens?
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Stomach acid induces sporulation causing production of toxin?
Colonization is not necessary Incubation time is 8-22 hours, symptoms last 24 hours Symptoms include diarrhea, cramps and pain; vomiting is rare Organisms can colonize the colon Acute hemorrhagic enteritis Invade other sites, giving rise to necrotizing infections (gas gangrene) Culture stool to confirm ; Oral rehydration |
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Describe clostridium cereus? What are the 2 toxins?
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Gram-positive, aerobic spore former
Ubiquitous soil organism Can cause a variety of infections Spores germinate in cooked food Two toxins = two forms of disease Diarrheal – formed in vivo 10-12 Hr Incubation Profuse diarrhea and pain Contaminated meat or vegetables Emetic - preformed 1-6 Hr Incubation Projectile vomiting Contaminated “fried rice” |
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What diarrheal disease do not require colonization?
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S. Aureus, botulism, bacillus, clostriduim perfringens
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What toxin is heat labile?
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botulism
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Hwo does cholera cause diarrhea?
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A-B toxin, causes excess cAMP production
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How are ETEC and EPEC different?
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EPEC does not make a toxin. It uses type III secretion to induce actin and prevent fluid reuptake
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What kind of diarrheea is associated with ETEC?
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secretory
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What causes gastroenteritis?
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salmonella and campylobacter
yersinia and vibrio parahaemolyticus |
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What causes dysentary?
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shigella, S. dysenteriae, e. coli O157
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What causes psuedomembranous colitis?
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clostridium difficule
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Which diarrheal systemic infection need antibiotics?
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s. typhi
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What diseases cause gastroenteritis? What are their reservoirs? What is their shared virulence factor? Which has a vaccine? Which affects only old people and children (not the cruise ship one)?
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Norovirus and rotavirus
humans and water Destroy cells at villus tip, cause shortened villi rotavirus rotavirus |
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Where do you find S. aureus?
What is the virulence factor? |
resident microbiota
superantigen toxin |
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Which kind of e. coli causes dysentery? What is the virulence factor?
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HUS (EHEC)
shigella like toxin |
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What are the respective virulence factors of ETEC and EPEC?
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ETEC- LT (cholera-like toxin and heat labile) and ST (heat stable)
secretory diarrhea EPEC- infants, actin rearrangement, malabsorptive diarrhea |
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What disease causes nosocomial diarrhea and psuedomembrane collitis? How do you diagnose the toxin?
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clostridium dificiles
ELISA |
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What disease hunts pregnant women and grows in the cold?
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Listeria monocytogenes
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What do shigella and EIEC (I = invasive) cause? What is the virulence factor?
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Type III secretion system promote uptake
Grows in cytoplasm Polymerizes host actin to move between cells |
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Why don't you want to use antimotility agents and antibiotics for shigella?
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infection can last longer
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Which diseases rearrange actin?
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EPEC, Shiga and EIEC, and listeria
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Which bacteria makes enterotoxin when in acid?
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clostridium perfiringens
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Why does norovirus live in cruiseships?
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low Id-50, Resists temps from 0-60°C
Persists in the environment Most disinfectants don’t work well Variation and non-protective immunity allow repeated infections |
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Which disease had a vaccine that caused intussusception that was pulled, but has two new vaccines?
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rotavirus
FUCKING ROTASHIELD |
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What are the protozoal parasites of the gastrointestinal tract?
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giardia intestinalis, cryptosporidium, entamoeba histolytica, toxoplasma gondii
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What protozoa causes steatorrhea? How?
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giardia intestinalis
Sucker disk damages intestinal cells |
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Which protozoa causes cholera-like diarrhea in AIDS patients?
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Cryptosporidium
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Which pin worm have egg antigens elicit allergic response and enemas?
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enterobius vermicularis
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What are the 2 forms of giardia? Which is replicating form and survival form?
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trophozoite- replicating
survival form- cyst |
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Which protozoa has a carrier form, invades the colon and lung, causes ulcers and granulomas, and caues small, blood stool?
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Entamoeba histolytica
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Which protozoal parasite lives in cats and attacks preggers and AIDS patients?
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toxoplasma gonadii
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Which worm can travel up to lungs and back to intestines? Where does it start?
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Ascaris lumbricoides
soil |
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What protozoa lives in dogs and causes skin and eye infections?
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Toxocara canis
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what are defenses of the CNS?
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Microglia (macrophages)
phagocytes and antibodies are low. |
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What causes the most damage in a CNS infection?
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host immune system
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What is septic vs aseptic CNS infection?
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Viruses and intracellular bacteria – “aseptic meningitis”
Increase in lymphocytes and monocytes Slight increase in protein levels Glucose levels constant Extracellular bacteria – “septic meningitis” Increased levels of neutrophils Protein levels increase significantly Glucose levels decrease Turbid |
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How does polio spread?
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lymphatics --> blood --> muscle --> PNs --> CNS
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What is the difference between salk and sabin vaccines?
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salk- killed vaccine (IgM)
sabin- live, oral (IgA) vaccine may revert and no longer used in US |
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What are the virulence factors of bacterial meningitis?
|
IgA proteases
Prevention of ciliary action Attachment structures |
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How does meningitis survive the blood? How does it go from mucosa to blood?
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capsule
endocytosis and tjctn damage |
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How does bacterial meningitis cross the BBB?
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capillary endothelial damage --> inflammation --> leaky
or monocytes |
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What causes neonatal meningitis?
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Group B strep (most common)
E. coli k-1 |
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What causes meningitis in adults? How does it spread?
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Streptococcus pneumoniae
lungs or sinuses --> blood |
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What causes meningitis in children?
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Haemophilus influenzae type b
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Where does N. meningitis start?
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throat or nasopharynx
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How do you diagnose meningitis?
What meningitis has small buds and thick capsule? |
bloog, glucose, protein, immune cells
strep pnuemon |
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African sleeping sickness – Trypanosoma brucei is spread by what?
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tsetse fly and Trypomastigote
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What is the best innate defense of the skin?
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sloughing dead cells
Viruses can’t live in dead cells Most bacteria that attach to skin cells carried away Thickness of dead cell layer prevents penetration by most microbes |
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What are the chemical defenses of the skin?
|
Lipids
Lysozyme Resident microbiota Produce antimicrobial substances Block colonization sites Especially important in hair follicles and pores Skin-associated lymphoid tissue (SALT) |
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How do you bypass skin defenses?
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puncture
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What are the 3 classifications of skin infections?
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exogenous, endogenous, and toxin
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What is the most common form of abcesses?
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staph Aureus
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What are the virulence factors of staph aureus?
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anti-phagocyte defenses, and hydrolytic enzymes
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what are the virulence factors of GAS or strep pyogenes?
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Antiphagocytic mechanisms
Hyaluronic acid capsule (antiphag) M protein – binds factor H (protects against complement) Surface protein similar to protein A (S. aureus) binds IgG in wrong orientation Hydrolytic enzymes – enhance spread |
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What does Folliculitis form?
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Microabscesses
Centered around a single hair follicle Can enlarge to form furuncles |
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What causes furuncles?
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S. aureus and may progress into carbuncles
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What is a carbuncle?
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Fusion of furuncle
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What is Erysipelas?
|
rash with sharp demarcation caused by GAS
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What causes Cellulitis?
|
Strep pyogenes GAS
FLESH EATING BACTERIA |
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What are the skin toxinoses?
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Toxic shock syndrome (superantigens)
Scalded skin syndrome (S. aureus) |
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How do you treat GAS?
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penicillin and debridement
|
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What do you get in bed sores?
|
bacteroides fragilis
They're fragile, bedridden people |
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How does clostridium perfringens get into wounds? why is it so bad?
How do you treat? |
spores
Gas gangrene and alpha toxin antibiotics, surgery, and hyperbaric oxygen |
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What gangrene does not involve gas?
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streptococcal gangrene
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What are the Dermatophyte infections?
What do they infect and what do they have |
Trichophyton, Epidermophyton, Microsporum
Keratinase Infect hair, skin, nails |
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What are tinea and kerion associated with?
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ringworm (dermatophytosis)
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hard painless nodule
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sporothrix
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What attacks burn victims?
|
Pseudomonas aeruginosa
Exotoxin A Hydrolytic enzymes Localized in blood vessel walls Resistant to many antibiotics Staphylococcus aureus |
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What ringworm (nematode) live sin water and can penetrate the body and migrate to the mesenteric vein resulting in hypersensitivity?
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Schistosoma
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How do diagnose Strongyloides stercoralis? Demographic? Cure? Source?
|
Diagnostic form is rhabditiform larva
Serious infections in immunocompromised patients especially military who served in SE Asia Difficult to cure Soil |
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What is a zoonoses?
|
disease between nonhuman vertebrates and humans
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What causes black death?
|
Yersinia pestis
pestis as in rat and flea. |
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How does lyme disease spread? What are the reservoir?
|
ticks to human (dead end)
deer and rats |
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What are the stages of lyme disease? How do you test?
|
lesion to dissemination to latent to tertiary
ELISA and western blots |
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What is Borrelia burgdorferi?
|
zoonoses with flagella
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What is ehrlichosis?
|
zoonose: deer to tick to mouse back to deer or to human
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How is malaria spread?
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enter through mosquito, sporozoites travel to liver, mature, then leave via mosquito again
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What are the symptoms of malaria?
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Fever and shaking chills
Occur at either 48 or 72 hours Due to lysis of red blood cells Lysis stimulates IL-1 and TNFa Anemia – due to lysis of RBCs Enlargement of spleen – due to spleen cells trying to clear infected RBCs, lysed cells and merozoites |
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What are the different types of
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P. vivax
Attacks occur at 48 hr Infects only reticulocytes Forms hypnozoites Persist in liver cells Break out of liver; start new cycle in RBCs Can survive for years and cause recurrent attacks P. falciparum Attacks occur at 48 hr Infects all stages of RBCs Convulsions Coma Hypoglycemia Pulmonary edema Shock Death No hypnozoites |
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What is the life cycle of Leishmania?
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sandfly to human to amastigote inside macrophage and then out via sandfly. Promastigote is the other form.
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What is inside a TB granuloma?
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dead cells, bacteria, epitheloid macrophages, lymphocytes, and fibroblasts
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What are the stages of TB infection?
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lungs --> macrophages --> granuloma --> lesion --> clearance or oh shit, TB is everywhere.
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What kind of stain IDs TB?
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acid fast stain
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What does the BCG vaccine protect?
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infants, but you lose skin test
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Who does thrush attack? Systemic?
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newborns and AIDS patients
not systemic |
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Where is Coccidioides? What does it form?
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california
lung granulomas |
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Blastomyces
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skin and lung fungus
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P jiroveci
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mild lung infection, except for immune compromised
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aspergillus
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Oral and lung
infections in compromised patients |
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How do you diff histoplasmosis and P. jiroveci?
Which have diff treatment for AIDS? |
Histoplasmosis and P. jiroveci infections
differentiated on appearance in bronchial washings |
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Corynebacterium diphtheriae
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toxin ADP ribosylates EF-2
possibly bloody psuedomembrane mainly heart damage, but others possible |
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Bordetella pertussis
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Causes pertussis (whooping cough)
adhesins A-B toxin causes cAMP increase Invasive adenylate cyclase LPS Peptidoglycan fragment Survival inside host cells |
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Strep throat
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Streptococcus pyogenes acquired from inhaling aerosols or eating contaminated food
Adheres to throat mucosa causing pharyngitis nonbloody throat pus patches Resolves in about a week May lead to complications |
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S. pyogenes
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b-hemolytic
Protein F – binds fibronectin Cell wall fragments Inflammatory Cause of symptoms of strep throat M proteins – prevent phagocytosis M-like proteins – bind Fc portion of antibodies and other host proteins Acute glomerulonephritis Rheumatic feverrheumatic heart disease |
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What are the 2 main reactions of S. pyogenes?
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Glomerular nephritis
Host makes antibodies to bacterial products Antigen-antibody complexes form Complexes deposited in glomeruli of kidney Type III immune reaction Rheumatic fever Host makes antibodies against M proteins Antibodies react with heart proteins Cytotoxic T cells trigger inflammatory response Type II immune reaction |
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How do you diagnose S. pyogenes (strep throat)?
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throat swab
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Streptococcus pneumoniae colonizaton routes
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eustachian --> ottis media
cilia damage (flu) --> lung damage --> capsule protects --> bacteremia |
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What is the main virulence factor of Streptococcus pneumoniae?
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antiphagocytic capsule
autolysins pnuemolysin |
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How do you treat S. pneumoniae?
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resistant to fluoroquinones and B-lactams
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Mycoplasma pneumoniae?
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walking pneumonia
5-15 year age cell wall conc on x-rays |
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Chlamydophila pneumoniae?
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Obligate intracellular pathogen
Cell wall has LPS but no peptidoglycan Spread by aerosols |
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Legionella pneumophila
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Grow in biofilms
Grow in macrophages diffuse on x-rays not gram stainable, but fluorescent |
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Vaccines against S. pneumoniae
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The conjugate vaccine doesn't have enough serotypes
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What does blood culture of s. pneumoniae?
|
possible septic shock. Normally in low numbers
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Pseudomonas aeruginosa
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capsule
toxin elastases Pyocyanin – damages endothelial cells |
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Bacillus anthracis
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aerosol
systemic macrophages carry to lymph nodes toxin and capsules |
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What are 4 intestinal parasites that cause localized infection?
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Giardia intestinalis
cryptosporidium parvum cyclospora cayetanensis enterobius vermicularis |
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What are the characterisitics of giardia intestinalis (protozoa)?
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localized
smelly, fatty diarrhea and flatulence trophozoite (replicating) and cyst (survival) forms sucking disc found in dirty water diagnosis: entero test and glycoprotein enzyme immunoassay |
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What are the characteristics of cryptosporidium parvum?
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contaminated water
watery, nonbloody stool diagnostic oocyst form no effective therapy, only rehydration sporozoites not self limiting in AIDS |
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What are the characteristics of cyclospora cayetanensis?
|
water and fresh produce
can be treated with antimicrobials |
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What protozoa parasite attacks HIV positive patients, does not cause PMN growth, water nonbloody stool?
How do you diagnose? |
cryptosporidium parvum
stool sample and enterotest |
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What is characteristic of enterobius vermicularis?
|
Scotch tape on anus will find eggs.
Warm water enema treatment, but now drugs. Pin worm. Immune response --> itch and rash. Dry out and explode releasing effs. Wash hands, clothing, and bedding. |
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What 4 parasites are invasive?
|
entamoeba histolytica
toxoplasma gondii ascaris lumbricoides toxocara canis |
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Entamoeba histolytica
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ameobic dystenery
90% asymptomatic and typically self-limiting colonize colon trophozoite and cyst can cause ulcers granulomas --> blood in stool lung infected hemotomously (suddenly invasive) diagnose with ELISA metraniazole |
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Toxoplasma gondii
|
lives in cats whole lifespan or undercooked food
becomes cyst outside of intestines serious w/ AIDS or pregnant woman tachyzoite invade, multiple, and rupture cells |
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Ascaris lumbricoides
|
only in humans
don't attach, but always swim upstream migrate to liver, heart, and lungs but then go back to intestines |
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Toxocara canis
|
dogs (puppies)
visceral larval migrans necrosis can be found in skin, granulomas, lung, or retina (serious) |
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Which parasites invade lungs?
|
toxoplasma or ascaris
|
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How do you diagnose:
giardia cryptosporidium enterobius vermicularis entamoeba histolytica toxoplasma ascaris toxocara |
trophozoites
oocysts tape trophozoites or cysts antibodies eggs eosinophilia, liver, or serological |
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What is Foxp3?
|
transcription factor for Treg
|
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What binds to influenza A?
|
sialic acid
|
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Why are respiratory tract/lung infections so dangerous?
|
diminished gas exchange
septic shock |
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What are 3 respiratory tract viral infections?
|
Rhinoviruses and influenza (common cold)
Respiratory syncytial virus (pneumonia) Adenovirus (common cold) |
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What does pertussis infect?
|
trachea and downwards
|
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What does RSV infect?
|
sinuses and pharynx + bronciotitis
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Where does rhinovirus infect?
|
sinuses
|
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Pico Noro is?
|
nonenveloped, +RNA;
|
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What binds to VP-1? What does it do? How does Zicam work?
|
ICAM-1
change conformation and inject RNA Zinc binds to ICAM-1, prevents virus from binding to host cell |
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What is influenza? Why does influenza predispose to future infections? What does HA of influenza bind to? What triggers influenza uncoating?
|
-RNA, enveloped.
damages mucus secreting, ciliated cells sialic acid moieties low pH (proton pump) |
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What are the 3 factors of influenza pathogenesis?
|
URI established
Targets mucus-secreting, ciliated and epithelial cells to remove this primary defense T cells and IFN are responsible for some of the pathogenesis BACTERIAL SUPERINFECTION (older people) |
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What can treat influenza?
|
Amantidine and rimantidine (affect the M2 ion channel -- see earlier chapter on virus uncoating)
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Most common cause of fatal acute respiratory tract infections in infants and young children?
|
RSV
|
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Which of the viruses are -RNA?
|
RSV
|
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How do you diagnose and treat RSV?
|
ELISA assay and respirators (no vaccine)
|
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What is adenovirus also used for?
|
gene therapy
|
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What are the symptoms of adenovirus?
|
Pharyngitis/respiratory disease (Ad types 1-7)
Gastroenteritis and diarrhea (Ad40, Ad42) Conjunctivitis (multiple types) Obesity (Ad 36) |
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How is adenovirus spread?
|
close quarters (barracks or school), shed in feces for long period, and noneveloped
|
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|
What are two secreted protectors of the urinary tract?
|
Tamm-Horsfall glycoprotein
Blocks adherence Lewis Antigen (ABO) Non-secretors are genetically predisposed to recurrent infection |
|
|
What causes most cases of cystitis and pyelonephritis?
|
e. coli
|
|
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What is the main virulence factor of UTI e. coli?
|
fimbriae
|
|
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How can e. coli give rise to long term infection?
|
pods
|
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What e. coli cousin is known for swimming, urease, and infectious kidney stones?
|
proteus
|
|
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What gives women toxin shock syndrome and extra-absorbent tampons?
|
staph aureus
|
|
|
Neisseria gonorrhoeae virulence factors? What are complications?
|
pilE/pilS and Opa
PID and perinatal infectio |
|
|
What are complications of Chlamydia?
|
PID and Lymphogranuloma venereum
|
|
|
Trichomonas vaginalis
|
wet mount --> twitching
doesn't really hurt males strawberry cervix |
|
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What is characteristic of bacterial vaginosis?
|
fishy odor
|
|
|
Why is chylamydia worse overseas?
|
invasive and blinding
|
|
|
What causes a direct escalation to neurosyphilis?
|
HIV
|
|
|
Why don't you give antibiotics to O157 patients?
|
Cells go lytic and toxin releases
|
|
|
How doe slisteria move?
|
cell to cell
|
|
|
What granuloma forming fungus is common in california?
|
Coccidioides
|
|
|
What fungal condition in the US, central, and south america causes skin lesions and budding lung lesions?
|
Blastomyces
|
|
|
What fungus doesn't cause granulomas, but infects the lungs? has an eosinophilic response, protein exudate, and honey comb appearance?
|
P. jiroveci
|
|
|
What forms lung fungal mats in immune compromised patients?
|
Aspergillus
|
|
|
What type of meningitis has a vaccine?
|
Haemophilus influenzae type b
|
|
|
What meningitis is common in adults and has a vaccine?
|
Streptococcus pneumoniae
|
|
|
What fungal infection causes meningitis?
|
Cryptococcus neoformans
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