Contribution Of Louis Pasteur In The Field Of Microbiology Flashcard
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| causes of bacterial meningitis |
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| -S. PNA (g. +) -H. Influenzae Type B (g. -) -N. Meningitidis (g. -) *all are encapsulated and can survive in the blood |
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| causes of neonatalbacterial meningitis |
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| -S. Agalactiae (g. +) -E. Coli (g. -) -L. Monocytogenes (g. +) |
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| gram + bacteria causing meningitis |
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| Strep PNA and Strep Agalactiae |
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| Bacteria causing Tetanus |
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| Clostridium Tetani |
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| Bacteria causing Botulism |
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| Clostridium Botulinum |
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| Bacteria causing Leprosy |
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| Mycobacterium Leprae |
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| clincal features of Bacterial (Acute/Purulent) Meningitis in Adults |
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| -SUDDEN fever -SEVERE HA -STIFF neck -pt may have flu like sxs initially and can be associated with n/v, AMS, photophobia, PETECHIAL rashes |
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| clinical features of bacterial meningitis in Newborns/Children |
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| -constant crying, poor feeding, sleeping constantly, irritability (all non-specific sxs) |
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| S. PNA is the leading cause of: |
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| -URI otitis media, pneumococcal PNA and Meningitis and conjunctivitis |
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| S. PNA distinguishing features |
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| -No Lancefield Ags -Alpha hemolytic -grows in pairs (cocci) -Optochin sensitive |
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| S. PNA virulence |
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| -Polysaccharide capsule -Autolysins (in cell wall) -Pneumolysins (in cytoplasm) |
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| Disease Mechanism of Pneumococcal Meningitis (caused by S. PNA) |
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| -usually in kids <2 and adults over 60 -starts as a focal infection in lungs, moves to blood, passes into CSF eliciting a strong macro/CK/Il-1 response |
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| distinguishing feature of Pneumococcal Meningitis |
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| Prolonged fever -sequelae: hearing loss and hydrocephalus |
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| Dx for Pneumococcal and Meningococal Meningitis |
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| -gram stain of CSF and f/u w/ bacterial culture -rapid test for Ags if pt has been tx'd with Immediate Abx Therapy |
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| Vaccine for Pneumococcal Meningitis |
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| Vaccine Conjugate Prevnar -2,4,6 12 months admin- very successful in kids under 2 yrs |
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| Characteristics of genus Neisseria |
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| -Gram Negative diplococci -non motile -Oxidase/Catalase positive -Aerobic- increased CO2 |
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| N. Meningitidis distinguishing features |
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| -ferments glucose AND maltose -can grow on standard media -POLYSACCHARIDE capsule with 13 serogroups |
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| N. Meningitidis serotypes: |
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| A: in developing countries- AFRICA/ASIA B: on the decline in the US C: increasing in the US W-135 and & *all can cause PNA, often the focal infection is unnoticed. Most ppl are just carriers; lives on MMM in URT |
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| N. Meningitidis virulence factors |
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| -Polysaccharide capsule -pili for adherence to nasopharynx -LOS; sialic acid addition (innactivating complement) -iGa portease and OMP's |
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| N. Meningitidis epidemiology |
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| -5-15% carrier rate -outbreaks common in winter, esp in dorms, military |
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| Disease Mechanism of Meningococcal Meningitis (caused by N. Meningititis) |
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| -spread by resp droplets (many healthy adults are carriers in URT and have protective Abs), the org adheres to non-ciliated columnar epithelium over 1-4 days causing a focal infection. Bacteria gets endocytosed , multiplies in submucosa and enters blood. Leads to meningitis or Septicemia (DIC) with hallmark PETECHIAL RASHES |
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| Vaccine for Meningococcal meningitis |
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| -Quadrivalent Vaccine (MCV4-2005) -for kids 11-12 yrs old and at risk pops -doesnt include serotype B bc its too similar to self proteins. |
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| H. Influenzae distinguishing features and dz mechanism |
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| -Pleomorphic gram neg. rod -growth on Chocolate agar with NAD and factor X -colonizes URT, transmitted by resp secretions often in NON_IMMUNIZED KIDS 1 mo-3 yrs often w/ otitis media then enters blood and eventually meninges |
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| H. Influenzae type B virulence factors |
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| -Polyribose capsule (not polysaccharide!) -IgA protease |
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| Dx of H. Influenzae |
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| -Gram stain CSF then f/u with culture on choc agar -immunological test for Abs to capsular ag -35% of isolates are resistant to ampicillin |
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| H. Influenzae vaccine |
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| Hib polyribose phosphate vaccine conjugate |
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| S. Agalactiae distinguishing features |
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| -gram + cocci -Beta hemolytic -Group B cell wall Ag (GBS) -ARROWHEAD streak on a plate with s. aureus -leading cause of neonatal sepsis and meningitis -resistant to bacitracin |
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| S. Agalactiae dz mechanism |
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| -colonies GI and vaginal/cervical MM w/o any sxs -transmitted to baby during birth (50%) |
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| S. Agalactiae infections |
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| -Early onset in neonates causing focal PNA--> bacteremia <7 days old -late onset >7 days--> meningitis |
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| E. Coli distinguishing features |
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| -Gram Neg rod -Facultative Anaerobe -Oxidase negative -ferments lactose; turns pink on MacConkey Agar |
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| E. Coli Virulence factors |
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| -Lipopolysaccharide O Ag -Flagellum H Ag -Capsule K Ag* -toxin production |
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| E. Coli Dz mechanism |
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| E. Coli moves from GI to vagina and transmitted to baby during delivery. Main presentation is meningitis (not PNA. the K Ag allows for adherence to brain endothelial cells) |
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| Listeria Monocytogenes distinguishing features |
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| -short, non spore forming, gram + rods -ubiquitous in the environment, intracellular parasite -tumbling motility at 23 deg C -contaminates cold cuts, soft cheeses -generally does not cause dz in healthy ppl (pregnant women are mildly immunocompromised) |
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| L. Monocytogenes dz mechanism |
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| -ingested by mother, expresses INTERNALIN to enter cells, makes LYSTERIOLYSIN O to destroy phagolysosomes, then multiplies and uses ActA to make actin to push through to neighbor cells and keep multiplying. |
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| L. Monocytogenes sxs |
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| -Gastro in healthy pts 48 hrs post ngestion -Bacteremia in pts with risk factors; fever, chills, myalgias -Meningitis in 5-10% of pts |
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| Listeriosis sxs in pregnant women |
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| -Bacteremia; flu like illness w/o CNS sxs -70-90% transmission to baby w/ 30 % mortality sue to disseminated dz and sepsis -if baby acquires it at birth, will dev meningits in 3-4 wks |
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| Features of Anaerobes |
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| -use fermentation to make energy -damaged by O2 -colonize in gut, distal ileum, lower genital tract, distal urethra, oral cavity and follicles of the skin |
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| characteristic of group Clostridum |
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| -Gram + rods -found in soil and GI tract -Anaerobic spore formers |
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| features of both C. Tetani and C. Botulinum |
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| -produce potent neurotoxins that exhert systemic effects -may cause death due to respiratory failure |
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| Clostridium Tetani distinguishing features |
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| -'tennis raquet' shaped spores; large rods -motile 'swarming' action on a plate -strict anaerobe- culture on blood agar -spores common in soil -cause dz in older ppl with waning immunity |
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| Clostridium Tetani virulence factors |
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| -Tetanospasmin toxin; has mealloproteinase that blocks release of inhibitory NTs. acts by cleaving synaptobrevin and increasing resting firing rate of motor neurons causing rigidity |
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| Clostridium Tetani disease mechanism |
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| Organism gets innoculated via a puncture wound, incubate 4-21 days. Spores release tetanospasmin toxin which gets taken up by retrograde transport into CNS. Toxin's heavy chain allows entry into neuron and light chain allows acts on synaptobrevin |
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| Clostridium Tetani sxs |
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| -lock jaw, progressing to opisthotonos, paralysis of chest muscles, respiratory failure and death |
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| Clostridium Tetani tx |
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| goal is to neutralize toxin with HTIG and abx. May need to debride the wound and give active immunization. |
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| Clostridium Botulinum distinguishing features |
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| -7 serotypes -spores found in soil, fresh water, surface of fruits/vegetables; like neutral and alkaline environments -produces Botulinum toxin |
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| Features of Botulinum Toxin |
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| -Most potent natural toxin, resistant to gastric enzymes -produces metalloproteinase to act on presynaptic membranes to block ACh release in PNS -inactivate by heating -commonly found contaminating home canned foods |
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| Botulism Intoxication sxs in an adult |
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| -present 12-36 hrs post ingestion -GI sxs, blurred vision, aphagia, progressive, bilateral, descending paralysis -NO FEVER OR AMS |
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| Botulism sxs in an infant 3 wks to 8 months |
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| -constipation, lethargy, poor sucking, paralysis 'floppy baby syndrome' -spores are able to germinate in the gut due to the alkaline environment then elaborate the toxin -up to 10 week incubation |
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| Botulism dx |
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| -clinical presentation -reportable dz -isolate and culture organism from specimens -the antitoxin is an equine trivalent and has the risk of hypersensitivity rxns |
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| Mycobacteria group distinguishing features |
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| -acid fast bacilli-stain pink with Ziehl Neelson Method -60% of their cell wall is lipid/mycolic acid; appears waxy when grown -grow slowly- 4-12 weeks on a plate -obligate AEROBES -non motile, non spore forming |
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| Mycobacteria group distinguishing features |
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| -acid fast bacilli-stain pink with Ziehl Neelson Method -60% of their cell wall is lipid/mycolic acid; appears waxy when grown -grow slowly- 4-12 weeks on a plate -obligate AEROBES -non motile, non spore forming |
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| Mycobacterium Leprae distinguishing features |
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| -causative agent of leprosy (Hansens dz) -low infectivity- need PROLONGED contact -CANNOT be grown in culture, only in armadillos and mouse foot pad at 30 degrees -can isolate from skin |
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| M. Leprae dz mechanism |
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| -transmitted via nasal secretions, enters body through mucosa or skin lesions. org gets taken up by macros- replicates and eventually enetrs schwann cells elaborating its PGL 1 virulence factor preventing fusion of phago/lysosome. body responds by bringing in lots of macros and lymphoctyes forming a granuloma |
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| M. Leprae sxs |
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| -chronic granulomatous dz -affecting PNS -Tuberculoid or Lepromatous Leprosy |
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| Tuberculoid Leprosy sxs |
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| -STRONG cell mediated immune response (few bacilli) -formation of granulomas ; large, flattened plaques on face, trunk and limbs with pale hairless centers. -Patchy anesthesia -Lepromin skin test will be + |
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| Lepromaous Leprosy |
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| -WEAK cell mediated immune response (lots of bacilli in skin and MM) -infectious -multiple skin lesions causing disfigurement; anesthesia, resporption of bone, thick and folding skin -NEGATIVE lepromin skin test bc T cell levels are so low |
