Micro Spring 2013 Block I – Flashcards
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| What pathogen is responsible for the majority of UTIs? |
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| E. coli |
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| What can increase the risk of ascending infection of UTIs? |
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| Use of a diaphragm and use of spermicides which increase vaginal colonization and adherence of E. coli and colonization of vagina with uropathogens |
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| What is cystitis? |
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| Infection of the bladder wall |
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| What are the symptoms of Cystitis? |
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| Frequency, urgency to urinate, dysuria, suprapubic tenderness, malodorous urine, bacteria and WBCs are common in urine |
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| What is pyelonephritis? |
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| An infection of the kidney and renal pelvis, most commonly following a bladder infection |
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| What is present in the urine in cases of pyelonephritis? |
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| WBCs, cellular casts, bacteria, and protein |
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| What is glomerulonephritis? |
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| Inflammation of the glomeruli in the nephrons |
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| How is glomerulonephritis detected? |
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| Glomerular capillary network becomes leaky allowing plasma protein and blood cells to be excreted in the urine |
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| Acute prostatitis is often an extension of what? |
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| Bladder or urethra infection and often follows urethral instrumentation such as catheterization |
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| What are pathogenicity islands? |
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| Genes for these virulence factors are linked together as multigene segments. Encodes for virulence protiens which are components of finbriae, pili, and outermembrane proteins |
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| What determines anatomical location of infection? |
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| Adhesive properties of virulence factors |
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| Pathogenicity islands are absent in what? |
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| Normal, fecal coliforms |
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| Pathogenicity islands are similar to plasmids in that they're what? |
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| Mobile |
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| Describe the appearance of E. coli |
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| Gram-negative rods |
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| What is the pathogenicity of E. coli? |
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| Adhere to mucosa via pili, causes tissue damage, endotoxin (LPS) causes inflammation |
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| How is E. coli treated? |
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| Penicillin or ciprofloxacin |
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| What is the function of the P-pilli for E. coli? |
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| allows bacteria to bind to P blood group antigens on urinary tract cells, especially kidneys |
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| What is the function of Type I pilli for E. coli? |
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| allows bacteria to bind to bladder, epithelium, and glycoproteins in various cells |
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| What is the function of the K1 antigen for E. coli? |
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| Impedes phagocytosis |
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| Describe the appearance of Proteus vulgaris and mirabilis |
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| Gram-negative rods |
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| What are the characteristics of Prtoeus vulgaris and mirabilis? |
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| Opportunistic, transmitted via catheters, uerase positive and HIGHLY MOTILE, can swarm across agar |
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| What is the second most common cause of UTIs behind E. coli? |
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| Proteus |
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| What is critical to the virulence of Proteus? |
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| Swarming ability |
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| How does Proteus precipitate the formation of calculi? |
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| Urease activity raises pH |
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| What anti-swarming agent can be used to inhibit the expression of virulence factors in Proteus? |
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| Para-nitrophenyl glycerol (PNPG) |
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| What is used to treat Proteus causing UTIs? |
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| Broad spectrum penicillins and cephalosporins |
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| Proteus shows resistance to what drugs? |
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| Nitrofurantoin and tetracycline |
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| Describe the appearance of Stpahylococcus saprophyticus |
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| Gram positive cocci |
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| What are the characteristics of Staphylococcus saprophyticus? |
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| Nitrate and coagulase NEGATIVE Catalase POSITIVE Novobiocin RESISTANT Nonhemolytic --> gamma-hemolysis |
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| Enterococcus faecalis can cause what types of maladies? |
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| Endocarditis, cystitis, wound infections |
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| Enterococcus faecalis is grown on what media? |
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| Blood agar (gamma hemolysis) and Bile-esculin agar (causes black discoloration) |
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| How is Enterococcus faecalis trated? |
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| Amoxicillin, Ampicillin, Vancomycin |
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| Describe the appearance of Klebsiella |
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| Gram negative rods, non-motile, forms large MUCOID colonies |
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| What protects Klebsiella from phagocytosis? |
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| K antigen |
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| What is used to treat Klebsiella infections? |
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| Cephalosporins |
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| What can increase the risk of Candida infections? |
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| Broad-spectrum antibiotics, pregnancy, diabetes, AIDS, surgery, indwelling catheters |
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| What most often causes a Candida infection |
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| Use of antibiotics that kill normal flora allow for infection |
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| What is used to treat Candida infections? |
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| Topical nystatin or clotrimazole |
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| What is necessary for Candida virulence? |
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| Germ tube formation which is induced by D-glucose and a pH of 7-8 |
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| What is th emost common site of nosocomial infections? |
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| Catheter associated UTIs |
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| The isolation of what pathogens would imply acquisition from an exogenous source due to their absence in normal GI flora? |
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| Serratia marcescens and Pseudomonas cepacia |
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| The majority of catheter associated UTIs are due to what? |
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| Endogenous bowel flora |
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| What might lead to precipitation of phosphatic salts, stone formation and eventual blockage due to growth on catheters? |
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| Microorganisms such as Proteus mirabilis |
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| A UTI caused by Schistosoma haematobium can lead to what? |
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| Renal failure due to obstructive uropathy, pyelonephritis, bladder carcinoma, may vacilitate the spread of STDs due to causative lesions |
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| How do you diagnose Schistosoma haematobium? |
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| Identify and speciate eggs in the urine over a 24hr urine collection. Watch for hasting at room temp if necessary |
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| How do you treat Schistosoma haematobium? |
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| Antihelmintics --> Praziquantel |
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| Dark brown to red urine suggests the possible presence of what? |
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| Porphyrins |
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| Black-brown urine suggests the presence of what? |
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| Melanins |
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| What is used to detect nitrites in urine? |
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| Griess' Reaction |
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| What do nitrites in urine indicate? |
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| Bacteriuria, though not all bacteria convert nitrate to nitrite, mostly gram-negatives |
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| The presence of leukocytes in urine indicates what? |
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| Leykocyte esterase activity in WBCs |
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| Blood in the urine indicates what? |
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| Pseudoperoxidase activity of hemoglobin |
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| How does yeast present in urine? |
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| Does not come up in lab testing, requires microscopic evaluation |
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| Hyaline casts in urine indicate what? |
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| Capillary membrane damage with proteinuria |
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| Most UTIs are treated with what? |
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| Amoxicillin (TMP-SX) and levaquin (fluoroquinolone) |
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| How are UTI's caused by chlamydia and mycoplasma treated? |
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| Tetracycline or doxycycline |
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| Nonsecreters are at higher risk for UTIs. How is secretion genetically determined? |
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| Presence of secretor gene (Se) is inherited independent of ABO and H genes responsible for A, B, and H antigens that are secreted. However, the H-gene is a necessary precursor for ABO, so all seretors will have the H gene |
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| Type I hypersensitivity reactions are mediated by what? |
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| IgE --> allergy, anaphylaxix, asthma, an immune response releases vasoactive and spasmogenic substances that act on vessels and smooth muscles |
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| Type II hypersensitivity reactions are mediated by what? |
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| Antibodies, promotes cell phagocytosis or lysis and cellular injury by inducing inflammation |
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| What are the classic examples of Type II hypersensitivity? |
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| Autoimmune hemolytic anemia and Goodpasture's syndrome |
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| How is Goodpasture's diagnosed? |
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| Antibody targeting non-collagenous domain of type IV collagen |
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| Type II hypersensitivity reactions always present in what way? |
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| Always localized, antigen is always fixed or bound to either cell, tissue, or ECM |
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| Type III hypersensitivity reactions are mediated by what? |
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| Immune response, antigen is NOT fixed, binds antibodies and induces inflammation, recruites leukocytes, is almost NEVER localized |
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| What is the only type III hypersensitivity reaction that is localized? |
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| Arthus reaction (Tetanus reaction) |
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| Type IV hypersensitivity reaction is mediated by what? |
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| Cell-mediated immune disorder via sensitized T-lymphocutes, Th1 lymphocytes/CD4, etc. Ex. contact dermatitis, MULTIPLE SCLEROSIS, type I diabetes, transplant rejection, tuberculosis |
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| What are the 3 criteria of autoimmune dissorders? |
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| Presence of autoimmune reaction Evidence that it is not secondary to tissue damage The absence of another well defined cause of the disease |
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| What is the dominant genetic factor that affects susceptibility to autoimmune disease/ |
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| HLA |
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| Reactive arthritis is associated with what gene? |
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| HLA-B27 |
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| What is central tolerance? |
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| Development of tolerance to self-antigens when encountered in PRIMARY sites of maturation such as lymphoid organs |
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| What is the function of AIRE (autoimmune regulator gene) in central tolerance? |
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| Encodes a transcription factor that normally induces hundreds of genes in the cells of peripheral tissues as well as the thymus which are recognized by T lymphocytes that then undergo NEGATIVE SELECTION, leaving only T-cells that do not recognize the self proteins |
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| A defective AIRE gene gives rise to what? |
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| Inherited autoimmune polyglandular disease (APD) or autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) |
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| What is peripheral tolerance? |
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| Development of tolerance when mature lymphocytes encounte rself-antigens in peripheral tissues |
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| What is anergy? |
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| Prolonged or irreversible functional inactivation of lymphocytes that encounter antigens in the periphery under specific conditions. A component of peripheral tolerance |
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| What is required for anergy? |
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| In absence of a second signal (CD28/B7) OR Inhibitory signal mediated via CTLA4/B7 interaction |
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| Where do regulatory T cells develop? |
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| In the thymus or in the periphery via recognition of self-antigens |
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| What mediates the development of regulatory T cells? |
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| IL-10 or TGF-beta secretion |
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| What gene is required for the development of regulatory T cells? |
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| Foxp3 gene |
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| A mutation in the Foxp3 gene causes what |
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| IPEX = immune dysregulation, polyendocrinopathy, enteropathy, X-linked |
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| How do regulatory T cells suppress autoreactive T cells? |
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| They recognize autoantigens presented in the context of MHC-II molecules |
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| What facilitates clonal deletion in peripheral tolerance? |
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| Fas/GasL interaction expressed by activated T cells that recognize self antigens, leads to apoptosis |
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| Mutation of the Fas gene results in what? |
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| ALPS = autoimmune lymphoproliferative syndrome |
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| What are the characteristics of ALPs? |
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| Lacks Fas molecules, cannot control size of lymphocyte population or remove autoimmune cells, secondary lymphoid organs cell and autoimmune reactions occur |
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| What are immune privileged sites? |
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| Tissues wher eantigens are hidden from the immune system due to lack of communication with blood and lymph. e.g. testes, eye, brain |
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| How does sympathetic opthalmia occur? |
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| Trauma to one eye results in release of intraocular protein antigens which are carried to lymph nodes and activate T cells. Effector T cells return and attack antigen in both eyes |
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| When immature B lymphocytes interact strongly wit self-antigens in the bone marrow, B cells are deleted via what process? |
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| Clonal deletion induces apoptosis |
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| What is clonal anergy? |
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| Autoreactive B cells in lymph nodes fail to receive T cell help or enter primary lymphoid follicles, are trapped in T cell zone and undergo apoptosis. When the migrate to periphery, they remain anergic, encounter T cell specific their autoantigens, and activates Fas/FasL to induce apoptosis |
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| As a rule, autoimmune diseases are never caused by what immunoglobulin complex? |
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| IgE |
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| The formation and deposition of soluble immune complexes in autoimmune disease corresponds to what type of hypersensitivity? |
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| Type III |
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| What causes complement activation leading to autoimmune hemolytic anemia? |
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| IgG and IgM abs binding to components of erythrocyte surfaces |
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| What are the 3 different means of RBC destruction in autoimmune hemolytic anemia following IgG/IgM binding induced complement activation? |
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| FcR+ cells in the spleen inducing phagocytosis Complement activation and CR1+ cells in the spleen inducing phagocytosis Complement activation and intravascylar hemolysis |
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| An uncommon autoimmune disease characterized by the presence of circulating autoantibodies targeting non-collagenous domains of the alpha-3 chain of type IV collagen is known as what? |
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| Goodpasture Syndrome |
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| The autoantibody targeting the alpha-3 chain of type IV collagen seen in Goodpasture Syndrome intiates inflammatory destruction of what? |
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| Basement membranes in renal glomeruli and lung alveoli |
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| How do you diagnose Goodpasture's syndrome? |
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| Linear IgG deposition on glomerular basement membranes and alveolar membranes detected by immmunofluorescence and the presence of anti-basememt membrane antibodies in the serum |
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| Both Goodpasture's and SLE autoantibodies show up on immunoflourescence. How are they distinguished? |
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| GPS is smooth, linear while SLE is lumpy/bumpy |
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| How is Goodpasture's treated? |
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| Primarily via **plasmapheresis. Also can prescribe *prednisone for immunosuppression of new Ab formation |
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| An autoimmune blistering disease that results from a loss of normal intracellular attachment integrity is known as what? |
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| Pemphigus |
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| What is the most common typ eof pemphigus? |
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| Pemphigus vulgaris |
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| How does pemphigus present? |
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| Initialy as oral ulcers that progresses to skin involvement. Primary superficial vesicles and bullae that rupture easily and leave shallow erosions covered with crust |
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| What is the main complication of pemphigus? |
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| Secondary bacterial infection and EXTREME loss of fluid** |
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| Which strain of pemphigus is wart-like and presents on the axilla, groin, and flexure surfaces? |
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| Pemphigus vegetans |
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| Which strain of pemphigus is benign and shows up on the scalp, face, chest, and back with a lack of bullae due to fragility? |
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| Pemphigus foliaceus |
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| Which strain of pemphigus is less severe and involves the malar area in lupus-like fashion? |
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| Pemphigus erythematous |
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| Pemphigus involves acantholysis which is the loss of attachment of what? |
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| Attachment between keratinocytes due to deposition of Abs against desmosomes** |
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| Pemphigus foliaceus deposits Abs that react with what? |
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| Desmoglein-1 present in the superficial layers of the epidermis |
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| Pemphigus vulgaris, the most common cause of pemphigus, deposits Abs that react with what? |
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| Desmoglein-3** present in deeper layers of the epidermis |
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| Rheumatic fever is a complication of what? |
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| Infection by Streptococcal pharyngitis or Streptococcal pyogenes |
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| What is the Jone's criteria of diagnosis? |
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| 2 major or 1 major + 2 minor criteria to confirm rheumatic fever |
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| What are the major Jone's criteria? |
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| Carditis, arthritis, chorea, subcutaneous nodules, arythema marginatum |
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| What are the minor Jone's criteria? |
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| Fever, joint pain, evidence of electrical changes in the heart |
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| How do you treat Rheymatic fever? |
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| 10 day course of penicillin |
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| Rheumatic fever most commonly damages which valves? |
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| Mitral (most common), aortic (2nd most common) |
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| A hyperthyroid state due to an autoimmune abs acting as agonists on TSH receptors is known as what? |
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| Grave's disease |
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| Grave's disease is biased towards which thyroid response? |
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| TH2 |
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| Graves disease commonly has what secondary manifestation? |
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| Hypertension |
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| Grave's disease is associated with what disease? |
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| HLA-B6 and HLA-DR3 |
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| Most patients with Grave's disease have what antibody in their plasma? |
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| TSH:receptor ab |
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| What are the symptoms of Grave's disease? |
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| Heat intolerance, nervouseness, irritability, weight loss, BULGING EYES, pretibial myxedema, tremor, enlarged thyroid |
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| What causes exophthalmous bulging eyes in Grave's disease? |
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| Increased volume of retro-orbital connective tissue and extraocular muscle due to proteoglycan and HA accumulation |
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| Graves disease shows what labs? |
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| Inc T3 and T4, dec TSH, increased TSH-r Ab and ANA levels w/o evidence of SLE |
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| How do you treat Grave's disease? |
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| Propranolol (symptomatic), Methimazole and Propylthiouracil (thyourea drugs) or thyroidectomy/ablation |
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| What disease is characterized as an autoimmune reaction against thyroid cells causing thyroid destruction and a hypothyroid condition? |
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| Hashimoto's Thyroiditis |
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| Hashimoto's Thyroiditis is notable in among thyroid disorders in that it is what? |
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| Most common thyroid disorder in the US |
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| How does Hashimoto's Thyroioditis usually occur? |
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| Infection or non-specific inflammation causes IGN-gamma to induce HLA II, a normally absent molecule, to be expressed on thyroid cells. Specific T cells induce an autoimmune response |
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| What are the symptoms of Hashimoto's Thyroiditis? |
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| Enlarged thyroid, depression, fatigue, dry mouth, dry eyes, thyroid antibodies |
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| What thyroid antibodies can be seen in Hashimoto's thyroiditis? |
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| Antithyroid peroxidase** (90%) Antithyroidglobulin** (40%) |
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| How is Hashimoto's thyroiditis treated? |
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| Synthetic thyroid |
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| Myasthenia Gravis is characterized by what? |
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| Blockade of AcH receptor by autoantibodies resulting in progressive muscle weakness |
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| What are the symptoms of myasthenia gravis? |
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| Dropy eyelids and double vision progressing to muscle weakness in the face to the trunk and extremities with possible breathing difficulty |
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| How is myasthenia gravis diagnosed? |
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| AcH ab detection and edrophonium test |
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| Type III hypersensitivity (immune-complex) is most often associated with what diseases? |
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| SLE and Hepatitis |
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| What is characteristic of SLE? |
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| Autoimmune response directed at autoantigens present in almost every cell in the body, has characteristic IgG abs which initiate inflammation, tissue destruction, and the release of soluble immune complexes |
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| How does SLE present? |
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| Butterfly shaped skin rash on face resembling a "wolf's head" due to deposition of immune complexes, may be provoked by sunlight |
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| What are the 2 most common symptoms of SLE? |
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| Glomerulonephritis and arthritis |
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| How does SLE cause glomerulonephritis? |
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| Hypercellularity due to proliferation of mesengial cells and endothelial cells in response to antigen-ab complex deposition |
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| How is SLE diagnosed? |
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| 40-60% have anti-DNA ab, 95% ANA-ab but this is NONSPECIFIC, 20-30% have anti-Sm (smith antigen), typically have HIGH IgG and LOW C3/C4 |
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| What drugs can induce SLE-like responses? |
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| Hydrallazin, Procainamide, D-peniccillamine, Isoniazid |
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| How does intermolecular epitope spreading of SLE occur? |
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| Q-specific T-cell recognizes same epitope present by MHC-II on all 3 types of B cells (P, Q, R). The reverse with B cells and P, Q, R T-cells canalso occur, helps recognize same epitope on different antigens |
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| How is SLE treated? |
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| High dose of Prednisone |
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| How is Chronic Discoid SLE different from classic SLE? |
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| Mimics skin manifestations by systemic manifestations are rare, anti-DNA ab is rarely present |
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| Skin biopsy shows deposition of what in pt with chronic discoid SLE? |
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| IgG and C3 at dermoepidermal junction (same as classic SLE) |
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| How is subacute cutaneous lupus erythematosus differentiated from discoid lupus erythematosus? |
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| Rashes are widespread, superficial, nonscarring, has mild systemic symptoms consistent with SLE, strong association with Abs to SS-A antigen with HLA-DR3 genotype |
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| Drug induced lupus has an extremely high frequency of what antibody? |
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| Anti-histone antibody |
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| Drug induced lupus is associated with what gene? |
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| HLA-DR4 allele |
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| What bacteria can cause acute glomerulonephritis? |
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| A complication of S. pyogenes infection |
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| Which types of S. pyogenes is nephrogenic? |
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| GAS type 12, 3, and 1***** Identification done based on M protein typing |
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| What characterizes Polyarteritis Nodosa (PAN)? |
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| Necrotizing inflammation of the walls of small/medium sized arteries (NO VEINS) |
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| Polyarteritis Nodosa is most likely associated with what diseases? |
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| HepB and CMV |
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| How is Polyarteritis Nodosa distinguished from Wegener's? |
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| Wegener's involves the lungs, PAN does not |
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| What are the important type IV hypersensitivity/autoimmunity (T-cell mediated) diseases? |
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| Type I diabetes, rheumatoid arthrytis, myltiple sclerosis, celiac disease |
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| What is the cause of Type I diabetes? |
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| Insulin an dglutamic acid decarboxylase (GAD) act as an antigen for T cell responses (type IV hypersensitivity) |
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| What viral pathogen may possibly increase the risk of type I diabetes? |
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| Rubella |
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| How is type I diabetes treated? |
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| Daily insulin injection |
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| What is the cause of multiple sclerosis? |
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| Autoimmune response against the myelin sheath of nerve cells causes demyelination of neuronal tissues in the white matter of the CNS (type IV hypersensitivity), causes sclerotic plaques |
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| What are the causative antigens for multiple sclerosis? |
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| All found in the myelin sheath: Myelin basic protein Proteolipid protein Myelin oligodendrocyte glycoprotein |
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| Multiple sclerosis is associated with what gene? |
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| HLADR2 |
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| How is multiple sclerosis treated? |
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| Initially with immunosuppressive drugs (corticosteroids) and injections of IFN-beta to prevent disease progression. Later more aggressive immunosuppressives such as cyclophosphamides are added alongside corticosteroids |
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| What is the cause of rheumatoid arthritis? |
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| A chronic systemic inflammatory disorder of unknown cause that principally attacks joints via inflammatory synovitis, causing permanent damage and ankylosis (bone fusion). A type IV hypersensitivity reaction |
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| What is rheumatoid factor? |
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| Antiimmunoglobulin antibodies that are produced against the Fc portion of human IgG. Not diagnostic, though prevalent in rheumatoid arthritis |
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| What is the classical presentation of patietns with rheymatoid arthritis? |
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| Affects proximal inter-phalangeal joints with polyarthritic fusiform swelling, is SYMMETRICAL, affects all hand and feet joints in chronic advanced stage |
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| What is the pathological hallmark of Rheumatoid arthritis? |
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| Pannus formation: a mass of synovial stroma consisting of inflammatory cells growing over articular cartilage that causes bone and joint destruction |
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| What are the major agents involved in pannus formation seen in rheumatoid arthritis? |
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| Cytokines IL-1 and TNF-alpha produced by macrophages and activated T cells induce inflammation |
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| What activates osteoclasts and promotes bone destruction in rheumatoid arthritis? |
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| Activated T cells and synovial fibroblasts producing RANKL, contributes to pannus formation |
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| What are rheumatoid nodules? |
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| Formations on the extensor surface of bone that are loosely affixed to underlying boney surface |
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| How is rheumatoid arthritis diagnosed? |
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| 4 out of 7 criteria: Morning stiffness Arthritis in 3+ joint areas Arhtritis in typical hand joints Symmetric arthritis Rheumatoid nodules Serum rh factor Typical radiographic changes |
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| How is rheumatoid arthritis treated? |
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| Anti-inflammatory drugs, immunosuppression, antibodies against TNF-alpha, and physiotherapy |
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| What causes celiac disease? |
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| Specific lesions of small intestines due to abnormal immune responses to gluten protein present in wheat (type IV hypersensitivity) |
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| What genes are associated with celiac disease? |
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| HLA-DQ2 and HLA-DQ8 |
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| T cells in celiac disease have receptors directed against what? |
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| Tissue transglutaminase complexes and proline-rich 33 amino-acid fragments, causes inflammation |
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| All patients with celiac disease have autoantibodies specific for what? |
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| Tissue transglutaminase Many also have anti-gliadin antibodies |
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| What are the symptoms of celiac disease? |
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| Diarrhea, flatulence, weight loss, fatigue, malnutrition, some skin manifestations are possible, adults become anemic and depressive, prone to intestinal cancer, children fail to thrive |
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| How is celiac disease treated? |
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| Gluten free diet |
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| What is the classic characteristic of Sjogrens syndrome |
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| Dry eyes and dry mouth |
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| What causes Sjogrens Syndrome? |
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| Lymphocitic infiltration of T cells and fibrosis of the lacrimal and salivary glands (type IV hypersensitivity reaction) |
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| What autoantibodies are present in Sjogrens? |
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| Rh factor, ANAs, SS-A, and SS-B (not diagnostic, all are also present in SLE) |
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| What are the symptoms of Sjogrens? |
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| Blurred vision, burning, itching, and accumulation of ocular secretions, cerostomia causes difficulty swallowing, reduced taste, enlarged parotid gland, dry mucosa, peripheral neuropathy |
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| How is Sjogrens treated? |
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| Symptomatic care, supportive care, artificial tears, sipping water, cholinesterase inhibitors and Ach derivatives may improve xerostomia |
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| White lesions unlike oral candiasis that cannot be removed by rubbing are what? |
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| Leukoplakia |
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| Leukoplakia with an erythematous component is known as what? |
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| Erththroplakia |
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| Lacy leukoplakia that may be erosive which requires a biopsy for diagnosis is known as what? |
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| Oral lichen planus |
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| Leukoplakia that eventually invades into the tongue mass is known as what? |
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| Oral cancer |
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| What causes leukoplakias? |
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| Chronic irritations from tobacco, dentures, excessive alcohol |
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| The majority of erythroplasias are either what? |
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| Dysplasia or carcinoma |
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| How is oral lichen planus treated? |
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| Corticosteroids, Cyclosporines, Retinoids |
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| What are some predisposing conditions for oral candidiasis? |
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| Oral dentures, chronic debilitating disease, diabetes melitus, chronic anemia, chemotherapy, immunosuppression |
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| How is Candida albicans diagnosed? |
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| Spore, non-septate hyphae, pseudo phyphae, and germ tube identification |
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| How is Candida albicans treated? |
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| Locally via nystatin mouth rinse and systemically with fluconazole or itraconazole if fluconazole resistant |
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| What is glossitis? |
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| Inflammation of the tongue with loss of filiform papillae leading to a red, smooth surfaced tongue |
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| Glossitis is usually secondary to what? |
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| Nutritional deficiency, drug reaction to ACE inhibitors, dehydration, irritants, autoimmune reactions such as Sjogrens or psoriasis |
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| Acute Necrotizing Ulcerative Gingivitis (ANUG or Trench Mouth) is found among whom? |
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| Young individuals under stressful conditions caused by mixed bacterial infections |
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| What are the characteristics of ANUG/Trench mouth? |
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| Painful gingival inflammation and necrosis, bleeding, halitosis, fever, cervical lymphadenopathy |
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| Synergistic infections between what types of pathogens is typical of ANUG/Trench mouth? |
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| Spirochetes and anaerobic bacteria such as Fusobacterium |
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| What causes ANUG/trench mouth? |
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| Stress, malnutrition, or immunodeficiency. Not contagious |
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| Fusobacterium pathogenesis is mediated by what? |
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| LPS |
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| How is ANUG/trench mouth treated? |
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| Clinamycin and 3rd gen Cephalosporin |
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| Aphthous ulcers/cancer sores/ulcerative stomatitis is caused by what? |
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| Uncertain, though association with HHV6 is suggested |
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| Where are cancer sores found? |
answer
| Non-karatinized mucosa, buccal and labial mucosa, NOT on gingiva or palate |
question
| What do cancer sores look like? |
answer
| Painful ulcers with irregular margin and yellow-grey fibrinoid center surrounded by red halo** |
question
| Cancer sores occur in relation to what? |
answer
| Stress |
question
| How are Aphthous ulcers/cancer sores/ulcerative stomatitis treated? |
answer
| Nonspecific, topical corticosteroids, oral prednisolone, thalidomide if recurrent in HIV patients** |
question
| What is noma, aka cancrum oris? |
answer
| Severe gangrenous stomatitis progressing beyond the mucus membrane to involve soft tissue, skin, and ocasionaly bone |
question
| What types of patients exhibit noma (cancrum oris) |
answer
| Severely debilitates patietns and people with poor oral hygiene, immunocompromised, malnourished, sometimes precipitated by measles |
question
| What are the etiologic agents of noma/cancrum oris? |
answer
| Fusobacterium, Bacteroides, and P. aeruginosa |
question
| What are the 3 clinical forms of oral herpes simplex? |
answer
| Recurrent small blisters on the lips (aka herpes labialis, most common type) Generalized oral infections (aka herpetic stomatitis) Small ulcers found on the palatal mucosa |
question
| What causes hand foot mouth disease in children under age 6? |
answer
| Coxsackie virus type A16 |
question
| How do you treat herpetic stomatitis? |
answer
| Acyclovir |
question
| What causes pharyngitis? |
answer
| An infection of the pharyngeal mucosa, most often viral (though bacterial is possible as well) |
question
| Which viruses are most likely to case pharyngitis? |
answer
| Rhinovirus, coronavirus, adenovirus, influenza, and EBV |
question
| What findings suggest a viral cause of pharyngitis? |
answer
| Mild pharyngeal symptoms with rhinorrhea, exudative pharyngitis, vesicular lesions and ulcers, conjunctival congestion, generalized rashes |
question
| What symptoms indicate a streptococcal infection behind pharyngitis? |
answer
| Fever, tender anterior cervical adenopathy, LACK OF COUGH, phayngeotonsillar exudate (3 or more to be likely) |
question
| Sreptococcus pharyngitis has what morphology? |
answer
| Gram positive oval cells growing in CHAINS, non-motile, lactic acid fermetator |
question
| Streptococcus pharyngitis grows best on what medium? |
answer
| Enriched blood agar |
question
| The virulence of Streptococcus pyogenes is mediated by what? |
answer
| Cell wall components, primarily M12 protein |
question
| What test can you use to quickly verify a strep infection? |
answer
| Rapid strep test or GAS rapid antigen detection test (RADT) These are solid phase ELISA tests |
question
| How is Streptococcus pharyngitis treated? |
answer
| Penicillin is first line, amoxicillin plus clavulanate to avoid failure with penicillin, erythromycin and second gen cephalosporin if penicillin sensitive |
question
| What causes diptheria? |
answer
| Corynebacterium diphtheriae |
question
| What is the morphology of C. diphtheria? |
answer
| Gram positive rod, non motile, exhibits CHINESE LETTER PATTERN, catalase positive |
question
| What is the most characteristic feature of diphtheria? |
answer
| Greyish-white membrane on the tonsiles that adheres to the underlying tonsils and is not easily removed, is made up of clotted blood and epithelial cells of host mucus membrane |
question
| The exotoxins of C. diphtheria are also found in what other pathogen? |
answer
| Pseudomonas |
question
| How is diphtheria diagnosed? |
answer
| Clinical diagnosis Definitive diagnosis via culturing on Tinsdale and Tellurite agar |
question
| How is Diphtheria treated? |
answer
| Diphtheria toxin anti-serum alongside penicillin or erythromycin. High mortality even with treatment |
question
| Describe the pathogenesis of Rhinoviruses |
answer
| Infects respiratory epithelium, causing them to lose their ciliary motion and slough off, injury causes inflammation, inducing acute symptoms. Inflammation eventually contains the infection |
question
| How is rihnovirus treated? |
answer
| Pleconaril is in trials, usually self limiting |
question
| Describe the morphology of adenovirus |
answer
| Non enveloped double stranded DNA virus that can remain infectious in environments for long periods but is easily inactivated by heat, chlorine, and disinfectants |
question
| What are the symptoms of adenoviral pharyngitis? |
answer
| Fever, runny nose, grey-white pus on pharynx and tonsils, enlarged cervical lymph nodes, conjunctivitis, and diarrhea |
question
| What symptom is present in adenoviral pharyngitis that is absent in the common cold? |
answer
| Enlarged cervical lymph nodes |
question
| How is adenovirus diagnosed? |
answer
| Lung biopsy and serologic testing |
question
| How is adenovirus treated? |
answer
| Self limiting |
question
| Describe the morphology of coronavirus |
answer
| Enveloped RNA virus with petal or club shaped spikes projecting from its surface giving it the appearance of a crown of thorns |
question
| What are the 3 types of human coronavirus? |
answer
| Etiologic agent for the common cold Enteric infections in the intestines Agent of severe acute respiratory distress syndrome (SARS) |
question
| What is essential for the diagnosis of pharyngitis? |
answer
| Pharyngeal pain and pain on swallowing (odynophagia) |
question
| When should a lateral neck X-ray be performed when suspecting pharyngitis? |
answer
| If pt has stridor or respiratory compromise to rule out laryngeal obstructions |
question
| What are the characteristics of Kawasaki's disease? |
answer
| Mucocutaneous lymph node syndrome most commonly affecting asian children younger than 5 |
question
| What are the disease characteristics of Kawasaki's disease |
answer
| Fever and four of the following for at least 5 days: Mucous membrane changes (injected pharynx, erythema, or strawberry tongue) Peripheral extremity changes (edema, desquamination, erythema, induration) A polymorphous rash Cervical lymphadenopathy Bilateral nonexudative conjunctivitis |
question
| When do you intervene with warfarin in cases of kawasaki's disease? |
answer
| If an aneurysm larger than 8mm in diameter occurs |
question
| What are the possible complications of bacterial pharyngitis? |
answer
| Peritonsillar or retropharyngeal abscesses, jugular vein thrombosis, rheymatic heart disease, post-streptococcal GN, acute airway obstruction, myocarditis, neuritis |
question
| What are some possible viral pharyngitis? |
answer
| Secondary bacterial infection |
question
| A peritonsillar or retrotonsillar abscess indicates what type of infection? Characteristics? |
answer
| Bacterial, usually as a complication of tonsillitis Tonsils should be ASYMMETRICAL, common ABOVE 5yo There is a danger of rupture and aspiration pneumonia |
question
| A retropharyngial or lateral pharyngeal abscess arises due to what? |
answer
| A complication of bacterial pharyngitis or accidental perforation of the pharyngeal wall by a foreign body, characterized by pain, inability to swallow, phonation change, and extended neck w/widened space Can rupture --> aspiration pneumonia, also osteomyelitis or acute mediastinitis Seen UNDER 5yo |
question
| What kind of x-ray finding do you see in a retropharyngeal/lateral pharyngeal abscess? |
answer
| Widening of space between cervical spine and posterior pharyngeal wall |
question
| What is first line in treatment of pharyngitis in children? |
answer
| Oral penicillin or amoxicillin in |
question
| What 2nd and 3rd line in treatment of pharyngitis in children? |
answer
| Erythromycin, if penicillin allergic giv clarithromycin, azithromycin, or an oral cephalosporin |
question
| What are the symptoms of rhinnitis? |
answer
| **Headache** Nasal congestion, post-nasal drainage (clear), Watery rhinorrhea, Sneezing Scratchy throat, pharyngotonsilar irritation (from drainage), General malaise |
question
| Why do sinus infections occur? |
answer
| When blockage occurs due to upper respiratory infection or viral rhinitis, the bacteria cannot be removed and are able to grow in numbers and cause an infection |
question
| The change from rhinitis to sinusitis is marked by what? |
answer
| Change from clear and watery to mucoid (yelow/green) rhinorrhea, marks the growth of the first aerobic bacteria |
question
| How often are cases of bacterial sinusitis polymicrobial? |
answer
| 1/3 |
question
| What fungal pathogens are possible (rare) causes of sinusitis? |
answer
| Candida spp. Aspergillus spp. Mucor spp. Rhizopus spp. Absidia spp |
question
| What are the symptoms of acute sinusitis? |
answer
| Usually of bacterial origin (aerobes anaerobes) More dental pain Children rarely complain of headache or facial pain Nasal discharge, congestion, facial pressure, postnasal drip, fever, cough, fatigue, ear pressure |
question
| How is sinusitis linked to smoking? |
answer
| H. influenza growth is stimulated by nicotine, thereby exacerbating infection in smokers |
question
| What are risk factors for sinusitis? |
answer
| Allergic rhinitis, Nasal trauma (including deviated septum), Immune compromised/diabetic, Smoking, Swimming/barotrauma, Nasal polyps, Cocaine abuse |
question
| How might Pseudomonas aeruginosa give someone sinusitis in a hospital setting? |
answer
| Common as a nosocomial infection from nasal tubes or catheters |
question
| What pathogen most commonly infects nasal passage hair follicles during a sinus infection? |
answer
| Staphylococcus aureus |
question
| What is the potential complication of fungal sinusitis? |
answer
| If invasive, will spread into CNS and eyes |
question
| Which strains of fungi that cause sinusitis are invasive? |
answer
| ? Rhizopus spp., Mucor spp., Absidia spp. |
question
| What is the most common complication of bacterial sinusitis? |
answer
| Preorbital swelling |
question
| What are some less common complications of bacterial sinusitis? |
answer
| Orbital cellulitis Subperiosteal abscess Orbital abscess Frontal and maxillary osteomyelitis Subdural abscess Cavernous sinus thrombosis Meningitis Brain abscess |
question
| How is sinusitis diagnosed? |
answer
| Clinical diagnosis. Cultures and x-rays are useless. MRI and CTscans may be useful in chronic or rare cases. Only clear useful diagnostic is transilumination |
question
| How do viral and bacterial cases of sinusitis differ? |
answer
| Fungal infections may affect only one sinus. Poor response to nasal decongestants (bacterial). |
question
| What are the two sites of ear infection? |
answer
| Otitis externa and Otitis media |
question
| How are ear infections contracted? |
answer
| Individual is exposed to environment that inhibits or removes cerumen and may also contain pathogens |
question
| What causes ear infections? |
answer
| 98% of cases are bacterial Pseudomonas aeruginosa (20-60%) Staphylococcus aureus (10-70%) Often polymicrobial |
question
| What is the hallmark sign of acute otitis externa ("swimmer's ear")? |
answer
| Tenderness of the tragus (when pushed), pinna (when pulled up and back), or both |
question
| What are the symptoms of otitis externa ("swimmer's ear")? |
answer
| Otalgia (70%), Itching (60%), fullness (22%), hearing loss (32%) |
question
| What was furunculosis? |
answer
| Infected hair follicle in outer third of ear canal, most commonly due to Staph aureus |
question
| What is otomycosis? |
answer
| Fungal infection of the ear canal, aka "tropical ear" Common in humid or tropical environments Causes: Aspergillus (60-90%), Candida spp. (10-40%) |
question
| What are the symptoms of otomycosis? |
answer
| Pruritis and thickened otorrhea (black, green, white) |
question
| How do you distinguish otitis externa from otitis media? |
answer
| Pneumatic otoscopy should show good tympanic membrane motion in AOE and absent or limited mobility in AOM Yellow/green = acute otitis media |
question
| What is malignant Otitis Externa? |
answer
| A complication of acute otitis externa seen in elderly, diabetics, or immune compromised Spreads to posterior cranial bone (osteomyelitis), soft tissue, middle ear, inner ear, and potentially the brai |
question
| What is the most common cause of malignant Otitis Externa? |
answer
| 90% Pseudomonas aeruginosa |
question
| How is malignant otitis externa diagnosed? |
answer
| Raised ESR, and abnormal CT/MRI (bone erosion) are diagnostic. Facial nerve paralysis may be an early symptom |
question
| How does an acute otitis media infection progress? |
answer
| Infection may spread from pharynx to middle ear (URT infection) Abrupt onset otalgia, irritability, otorrhea, or fever Infection is treated or pressure from bacterial growth bursts tympanic membrane |
question
| Acute otitis media must be differentiated from what? |
answer
| Otitis media with a clear effusion, a non-infectious condition of the middle ear |
question
| When is the peak first incidence of acute otitis media? |
answer
| 6-9 months |
question
| What are some risk factors for acute otitis media? |
answer
| Bottle fed, Smoking parents, Attending daycare, Male |
question
| How is acute otitis media diagnosed? |
answer
| Rapid onset (48 hours*) Presence of middle ear effusion Signs and symptoms of middle ear inflammation |
question
| What is Chronic Suppurative Otitis Media? |
answer
| Chronic inflammation of the middle ear and mastoid mucosa in which the tympanic membrane is NOT intact and discharge (otorrhea) is present |
question
| What causes Chronic Suppurative Otitis Media? |
answer
| Untreated acute ototis media |
question
| What causes Cholesteatoma? |
answer
| Prolonged eustachian tube dysfunction, leading to negative pressure that draws the upper flaccid portion of the TM inward. This creates a squamous epithlemium lined sac. When the opening becomes blocked/clogged this can lead to chronic infection |
question
| Cholesteatoma usually leads to what complication? |
answer
| Bone erosion |
question
| How is Cholesteatoma diagnosed? |
answer
| Physical examination reveals an epitympanic retraction pocket or perforation that exudes keratin debris |
question
| What is a complication of cholesteatoma? |
answer
| Osteomyelitis/ Mastoiditis Meningitis Brain Abscess Dural Sinus Thrombosis (DST) Otitic Hydrocephalus Otitis Externa (most common) |
question
| What is Labyrinthitis? |
answer
| Acute onset of continuous, usually severe vertigo lasting several days to weeks, along with hearing loss and tinnitus Cause is unknown but frequently follows upper respiratory tract infections |
question
| What are some ear problems associated with multiple sclerosis? |
answer
| Episodic vertigo and chronic imbalance. Hearing loss is usually unilateral with rapid onset that may abate spontaneously |
question
| What causes "honeymoon cystitis"? |
answer
| Staphylococcus saprophyticus |
question
| Which HLA genes are associated with Addison’s disease, Graves’ disease and myasthenia gravis? |
answer
| HLA-DR3 |
question
| A patient presents with complaint of coughing up of blood and blood in urine. Which of the following is the most likely mechanism of this autoimmune disease pathology? |
answer
| Antibody deposition on both glomerular and alveolar basement membrane |
question
| You order a CBC on a patient suspected to have urinary schistosomiasis. What should you be checking for? |
answer
| eosinophilia |
question
| The main reason Escherichia coli is the most common cause of UTIs is that it is what? |
answer
| an enteric bacterium |
question
| What are the effects of urease activity by proteus mirabilis? |
answer
| Hydrolyzes urea, produces ammonia and carbon dioxide, raises pH precipitating the formation of calculi stones |
question
| Enterococcus faecalis is strongly associated with what bacterial infection? |
answer
| Endocarditis |
question
| Enterococcus faecalis is grown on what? |
answer
| Blood agar Bile-esculin agar (black discoloration) |
question
| Enterococcus faecalis acquires 25% of its genome through what means? |
answer
| Lateral gene transfer between Staphylococcus and Streptococcus Pathogenicity island located on genome produce toxin that forms holes in cell wall and allow for adherence |
question
| Enterococcus faecalis has high antibiotic resistance due to what? |
answer
| Ability to acquire mobile gene elements |
question
| How is Enterococcus faecalis treated? |
answer
| Amoxicillin Ampicillin Vancomycin |
question
| UTI caused by Salmonella sp. is suspicion for what? |
answer
| Urinary schistosomiasis |
question
| What are the statistics associated with recurrent UTIs? |
answer
| 20% of women who contract a UTI will suffer another Of these women, 30% will suffer additional UTIs |
question
| What causes Sub-acute bacterial endocarditis? |
answer
| Infection of the damaged valves by normal flora of mouth (Streptococcus viridans) and skin (Staphylococcus epidermidis) |
question
| Graves Disease is associated with what genes? |
answer
| HLA-B8 and HLA-DR3 |
question
| Thickening of basement membrane in SLE is due to what? |
answer
| Immune-complex deposition on the basement membrane The clinical correlate is proteinurea and microscopic hematuria |
question
| The most common causes of death from SLE are what? |
answer
| Renal failure and intercurrent infections |
question
| Does P-ANCA or C-ANCA present in polyarteritis nodosa? |
answer
| P-ANCA |
question
| In 90% of MS patients, the sclerotic plaque contain plasma cells that secrete what? |
answer
| Oligoclonal IgG into the CSF |
question
| Rheumatoid arthritis is most often associated with what gene? |
answer
| HLA-DRB1 |
question
| Patients with Sjogren syndrome have an approximately 40-fold increased risk of developing what? |
answer
| Lymphoid malignancies |
question
| Some patients with limited scleroderma develop a combination of symptoms referred to as CREST which stands for what? |
answer
| Calcinosis, Raynaud phenomenon, Esophageal dysmotility, Sclerodactyly, & Telangiectasia |
question
| Reiters syndrome (reactive arthritis) is a clinical tetrad of what symptoms? |
answer
| Urethritis Conjunctivitis (or less commonly uveitis) Mucocutaneou lesions Septic arthritis |
question
| Reiters syndrome usually develops following what kind of infection? |
answer
| Dysenteric infection (with Salmonella, Shigella, Yersinia, or Campylobacter) or a sexually transmitted infection (with Chlamydia trachomatis, or perhaps Ureaplasma urealyticum) |
question
| What is the clinical presentation of Reiters (reactive arthritis)? |
answer
| The arthritis is asymmetric and involves the major weight bearing joints fever, weight loss The mucocutaneous lesion include balanitis, stomatitis, keratoderma blennorhagicum Most of the symptoms but arthritis subsides within weeks |
question
| How is Reiter's treated? |
answer
| Non-steroidal anti-inflammatory drugs are the main drugs used Tetracycline in reactive arthritis with C. trachomatis reduce the duration of symptoms Sulfasalazine and anti-TNF agents are tried in patients refractory to NSAID and tetracycline |
question
| What are the most common forms of amyloid protein? |
answer
| AL (amyloid light chain): is derived from plasma cells and contains immunoglobulin light chain AA (amyloid-associated): is a unique non-immunoglobulin protein synstesized by the liver Ab amyloid: found in the cerebral lesion of Alzheimer disease |
question
| How do you differentiate Group A from Group B Strep? |
answer
| Group A strep is bacitracin sensitive |
question
| What is the pathological hallmark of Kawasaki’s Disease? |
answer
| IgA plasma cell infiltration in the visceral organs, lungs, and coronary arteries |
question
| What can be given for influenza post-exposure prophylaxis |
answer
| Amantidine |
question
| What causes Acute Laryngitis? |
answer
| Infection of the larynx that results in an inflammatory reaction Most often viral but can also be bacterial |
question
| Lateral X-rays help exclude what when diagnosing acute laryngitis? |
answer
| Acute bacterial epiglottitis Bacterial tracheitis |
question
| What should be performed when hoarseness persists longer than 2 weeks with acute laryngitis? |
answer
| Direct laryngoscopy |
question
| What causes Croup (Acute Laryngotracheitis)? |
answer
| Subglottic inflammation and edema caused by a viral or bacterial infection of the larynx, trachea, and bronchi |
question
| What is the most common cause of upper respiratory tract obstructionin children between the ages of 6 months to 6 years |
answer
| Croup (Acute Laryngotracheitis) |
question
| What is the most common cause of croup in children? |
answer
| Parainfluenza virus type I and II Influenza A or B RSV |
question
| What is the most common cause of croup in adults? |
answer
| HSV Influenza A or B |
question
| What are the signs and symptoms of croup? |
answer
| Hoarsness of voice Brassy cough Stridor, Fever, Rhinorrhea Ronchi, crepitations or wheezing Diminished breath sound |
question
| Imaging shows what in patients with croup? |
answer
| Narrowing of the air column |
question
| How is Croup treated? |
answer
| Cool air humidification Racemic epinephrine Dexamethasone Intubation may be required if medical management fails Antibacterial if bacterial |
question
| What is Acute Epiglottitis? |
answer
| Respiratory emergency acute inflammation and edema of the epiglottis and can cause upper airway obstruction More common among children between 2-6 years of age Bacterial only |
question
| What causes acute epiglottitis? |
answer
| H. Influenzae type b S. Aureus S. Pneumoniae S. pyogenes |
question
| What are the symptoms of acute epiglottitis? |
answer
| Short, rapidly progressing febrile illness Sore throat (esp. in adults) Dysphagia Shortness of breath Anxious looking and appears toxic Forward leaning with neck extended posture Drooling and muffled voice May have a stridor |
question
| What can aid in rapid diagnosis of acute epiglottitis? |
answer
| Serum latex agglutination test for Hi type b |
question
| What imaging sign do you see in acute epiglottitis? |
answer
| Thumb sign |
question
| Hemophilus influenzae grows best on what? |
answer
| Chocolate agar media Requires hematin (X factor) and NAD (nicotine adenamide diphosphate, V factor) for growth |
question
| Describe the pathogenesis of Hemophilus influenzae |
answer
| Pili and other adhesins bind to epithelial cells Grows between the respiratory epithelial cells The capsule inhibits opsonization and phagocytosis Endotoxin is locally toxic, but does not cause endotoxemia No exotoxins |
question
| Coccobacillus growing on chocholate agar but not on blood agar strongly suggest what? |
answer
| Hemophilus |
question
| What kind of prophylaxis is available for Acute epiglottitis and pneumonia? |
answer
| Rifampin Infants are protected by maternal antibody up to 6 months of age Antibody response to Hib PRP is poor in children less than 18 months of age |
