pathology of infectious diseases I - lecture notes - julia Flashcards
what are the epithelial barriers to disease in the different regions where disease can enter (meaning what types of cells in the skin, resp tract, GI tract, genitourinary tract)?
epithelial surfaces
- skin - stratified squamous epithelium
- respiratory tract - ciliated columnar epithelium
- GI tract - columnar epitheilium with mucous secretion
- genitourinary tract - squamous and columnar epithelium, plus urinary epithelium - have specific receptors on them and some organisms have specialized themselves to adhere to them
what sorts of bacteria will be in an anatomic site?
the normal flora, which varies based on the site potential pathogens opportunistic pathogens
what can be the negative consequence of antibiotics on the normal flora?
can disturb the normal balance of bacteria by killing some of the ones we want to live
what are opportunistic pathogens? what are some examples?
- largely sit in our normal flora, hardly ever cause disease, unless the host has some major defect in immune mechanisms
- they require some opportunity to become disease-causing eg pneumocystis jirovecci
- usually in peoples lungs - discovered when AIDS became common cytomegalovirus
- 70% of us have been exposed, might have had a cold or something, but if people have immunosuppression, can reactivate and cause severe and potentially lethal disease
what are potential pathogens? what is an example?
organisms capable of causing disease but can also sit around on mucosal surfaces and do nothing and be part of the normal flora but can break out of that and cause disease eg. streptococcus pneumonia
what are obligate pathogens? what is an example?
bacteria that, if they’re there, they always cause disease - not part of the normal flora bordetella pertussis
how do bacteria invade?
usually through epithelium or into organs some can invade into individual cells
what are virulence factors?
toxins that bacteria produce that make them capable of causing disease
what are endotoxins?
virulence factors often in cell walls - lipopolysaccharide
what are exotoxins?
virulence factors that are secreted - may mimic intra cellular signaling molecules
what are adhesins?
virulence factors that allow bacteria to adhere to cell types
what types of enzymatic virulence factors can be made?
- proteases
- collagenases
- phospholipases
all can disrupt cells and tissues
how do bacteria and host cells compete for nutritional factors?
- major one appears to be iron
- bacteria release virulence factors that include iron binding proteins
what is hepicidin?
appears to be the major protein regulating iron levels - peptide hormone that depresses the amount of iron that’s available
what is acute suppuration?
production of pus - acute inflammation
what are some forms of acute suppurative inflammation?
- pnemonia
- endocarditis
- pyelonephritis
- appendicitis
what cells are involved in acute suppartive inflammation?
polymorponuclear leukocytes - cause production of pus
what causes bacterial pneumonia?
streptococcus pneumoniae has polysaccharide capsule - main virulence factor prevents phagocytosis makes proteases that breaks down mucosal antibodies has cell wall
what are the steps in the progression of pneumonia?
- normal colonizer invades bloodstream (bacteremia) or tissue (pneumonia, menigitis)
- recruitment of PMNs at the site of infection by integrin-mediated (CD18) and other processes
what will lobar pneumonia look like? (xray, gross)
large white area in one lobe of lung when fixed, lobe will be light, dense, not spongy as it should be = consolidation
what will the edema stage of pneumonia look like histologically?
- serous exudate
- protein-containing fluid leaks out of vessels
- alveoli are filled with pink fluid
- if look at excudate, will be PMNs, gram positive bacteria, often in pairs
what does the acute inflammation stage of pneumonia look like histologically?
- see series of other cells being recruited
- lots of cells with irregular nuclei = PMNs
- cells with more cytoplasm probably macrophages - but they’re not the predominant population
- vessels become congested - lots of RBCs in what should be really thin vessel walls
- granular pink stuff = serous fluid - was already pink - major protein in that begins to be activated by all of the parts of coagulation cascade and begins to coagulate into fiber so get pink clumps - important to allow PMNs to have something to move on
what does the resolution stage of pneumonia look like?
- alveolar wall not quite normal yet
- most of the inflammatory cells are macrophages cleaning up the dead cells, debris, fibrin
- normal architecture of alveolar space left
what should the mitral valve look like? what does it look like with endocarditis? (gross)
thin and glistening
if infected, covered in yellow stuff
what does a normal valve look like histologically?
mostly collagen, underlayed by fibrous and mucsuloskeletal structure
what does a valve with endocarditis look like?
- lighter pink = fibrin
- darker pink = collagen of valve
- dark smudges/irregular blue clumps = inflammatory cells or masses of bacteria
what will periphearl emboli due to endocarditis look like?
painful nodules that you can see
can also see lesions in small vessels in retina
what does a septic infarct look like? what can cause it?
- clump in vessel, bacteria and inflammatory inflitrate around it
- emboli from endocarditis
what does pyelonephritis look like histologically?
- interstitial inflammation (in area between collecting tubules)
- lots of PMNs
- glomerulus won’t be really involved since this doesn’t come through the vascular channels
- collecting tubules will be full of PMNs, then these will get out into the interstitium
what does apendicitis look like?
- serosal inflammation
- mucosal wall being shredded, coming off
