Mcb Test 3

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Acid fast organism can't be stained because of? What is the mordant for acid fast organisms?

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Thick waxy coat allowed them not to be stained. Heat is the mordant.

Ex-myobacterium (TB and leprosy).

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Why are gram neg bacteria more resistent to treatment?

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They have an outer membrane with very selective porins in them.

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Gram staining gives you

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gram reaction, morphology, arrangement

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Examples of Gram pos Cocci

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Steph- in chains
Staph- in clusters

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Gram neg Cocci example

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N. Gonorrhea

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Gram + bacilli examples

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Bacillius and Clostridum. Both have endospores and long chain rods. Bacillius is aerobic and Clostridum is an obligate anerobe ( it can grow deep in body).

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Gram - Bacilli examples

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Enterobacteriaceae, short rods that cause many dx. E.Coli, Shingella and Salomonella.

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Tests used for rapid detection of microorganisms

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1.Light or electrommicroscopy (with or without stains)
2.Immuno test
3.Nucleic acid test
4.Polymerase chain reaction (PCR)

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Direct assay Microscopy

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Gram Stain, Acid fast stain, direct microscopic examination (like dark field),wet mount (no stain).

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Direct Assay Immunological

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ELISA test, RIA test. both are not time consuming and can detect both infectious and non infectious materials

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ELISA test

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quantitative and qualitative test. Can detect antigen or antibody.

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Direct Assay Nuceli Acid probes

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The most acurate test. DNA or RNA segments are labeled and probe reacts with homologous species of microbial genomes.

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PCR test

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rapid, sensitive, amplifies specific segments of DNA and RNA. Specificty can vary.

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Immunological test

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test serum for specific Ab, disgnose current or recent infection. Used for epiemiological stuides. Uses anti-serum to ID bacteria. Test is based on aggulatination.

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Direct flourescent antibody test

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Antibody labeled with flourescein isothiocynate, Can detect the direct infection of the antibody.

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Indirect fluorescent antibody test

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uses two antibodies; the first (the primary antibody) recognises the target molecule and binds to it, and the second (the secondary antibody), which carries the fluorophore, recognises the primary antibody and binds to it. This protocol is more complex than the primary (or direct) protocol above and takes more time but allows more flexibility.

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polyclonal antibodies

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antibodies that are obtained from different B cell resources. They are a combination of immunoglobulin molecules secreted against a specific antigen, each identifying a different epitope. Made from mammals who are immunized.

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Monoclonal antibodies

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one type of antibody with one specific binding site.

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PCR can detect

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virulence genes and toxin genes. Primers can be used to isolate the specific gene you want.

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Gram + spore-forming anaerobic bacilli

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Clostridium perfringenes, clostridium tetani, clostridium botulinum, clostridium difficile.

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Why are gram + spore forming anerobic bacteria so harmful to humans?

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1. they produce the most toxic chemicals known to humans (neurotoxinc and endotoxins)
2.spread rapidly w/o oxygen
3.all virulence factors including the endospores
4. all gram pos with long chained rods, have endospores, and are obliagte anerobes.
5.ubiquitous
6. some are part of normal flora

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physical effects of gram + spore forming anerobic bacteris

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Most are related to GI dx, gangreen, explosive diarrhea, skin infections,food poisioning, and some disrupt the normal neural functioning (tetanus and botulism), some are resistant to antibiotics.

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Clostridium difficile associated diarrhea (CDAD)

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usually affects children. Hard to grow and ID in lab.

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Complications of clostridium difficile

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Can be asymptomatc. Antibody-antigen diarrhea, pseudomembranous colitius, toxic megacolon, CDAD.

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reservoirs for toxigenic C.difficile

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up to 70% of healthy neonates about 3% adults and 15% hospitalized pts. Most-dx causing strains are acquired from outside such as hospital env or HCW hands. Part of normal flora and a nosocomial infection.

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Diagnosis of CDAD

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Endoscopy, culture, cell culture cytotoxin test, E1A toxin test, PCR toxin gene detection.

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Treatment for CDAD

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1.discontinue or modify offending agent
2.replace fluid/electroclytes
3.do not treat asymptomatic
4. do not treat non-socomial diarrhea w/o testing. Relapse occurs in about 20% of pts.

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Relapse

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is recurrent dx with the same strain

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Clostridium perferinges

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Two forms of exotoxins (alpha/beta). Alpha toxins kill the human cells because it grows rapidly and prds gas.

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Gas Gangrene

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Clostridial myonecrosis. Muscle swelling, cuts oxygen supply, severe pain, sepsis, gas prd, ischemia.

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Botulinum toxin

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Clostridium botulinum, very neurotoxic. Bac does not need to enter the system.Can be transmitted thru honey.

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Beta hemolysis

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reaction that kills the RBCs completely. Used to catergorize bacteria.

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Alpha hemolysis

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partially kills RBCs. Used to categorize bacterias.

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Alpha Hemolysis seen in which bacteria

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Strepococcus Pneumonia and Virdians

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Beta hemolysis seen in which bacteria?

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Strep Pyrogens, Clositridium perf, staphylococcus, strep alga.

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streptococcus spp.

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Gram + bacteria. Most common infectious organism to humans the most common being strep pyogenes. All has fastidious and some are capnophilic.

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Classification of beta streptococci

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Based on C-carbohydrate antigenic analysis.
1. group a- pyogenes (AP)
2. group b- agalactiae (BA)
*strepococcus pneumoniae is alpha hemolytic and has no group.

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Group A streptococci

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gram pos, causes mild to life-threatening dx such as skin and respiratory infections. Also causes invasive systemic infections by growing in the body and spreading thru the blood and later causes damage to several parts of the body.

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Examples of Group A streptocci infections

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strep throat (pharyngitis), tonsilitis, scarlet fever, rheumatic fever, impetigo, cellulitis,necrotizing fascitis.

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Virulence factors of S.pyogenes

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1. pili,
2. M protein (anti-phagocytic protein on cell membrane),
3.capsule,
4. hyaloronidase (spreading factor),
5.pyogenic
6.strep s and o
7. pyogenic exotoxins
8. bacterimia (microbes spread thru the blood)

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Hyaloronidase

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an enzyme that destroys CT.

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Streptolysins S and O

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most viscous virulence factors. kill all kinds of cells. Beta hemolytic activty, cause immune response and kills a bunch of cells in the immune system.

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Strep throat

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manifest-pain, pharnygeal erythema, sore throat, fever, malaise. Can treat with antbiotics.

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Erysipelas

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local inflammation of skin and subcutaneous tissue. Redness all over skin.

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Impetigo

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Fluid, pus, scabs over body, easilye treated and usually found in children. Can also be caused by staph.

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Hyaloronidase

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an enzyme that destroys CT.

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Streptolysins S and O

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most viscous virulence factors. kill all kinds of cells. Beta hemolytic activty, cause immune response and kills a bunch of cells in the immune system.

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Strep throat

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manifest-pain, pharnygeal erythema, sore throat, fever, malaise. Can treat with antbiotics.

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Erysipelas

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local inflammation of skin and subcutaneous tissue. Redness all over skin.

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Impetigo

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Fluid, pus, scabs over body, easilye treated and usually found in children. Can also be caused by staph.

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Scarlet Fever

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rash, face flush, whitish coating on tongue. Not deadly any more.

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Rheumatic fever

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carditis, polyarthritis, chorea, erytherma margination, suncutaneous nodules. Can cause heart problems.

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Necrotizing fasciitis

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within 1 day- pain, flu like symptoms.
3-4 days-swelling, dark marks, blisters with black fluid
4-5 days- BP drops a lot, toxic shock, unconscious. Flesh eating bacteria.
This kills fascia muscle, once this layer is removed necrosis occurs. PCN works best for this infection.

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How to diagnose Group A strep

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throat culture (7-10hours for results) or rapid antigen test (highly specific and gets results in minutes).

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Group B streptococci infections

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1.strep agalactiae
2.strep pneumoniae

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Streptococcus agalactiae

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beta hemolytic, gram pos, causing puerperal sepsis,pneumonia and meningitis

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Virulence factors of group b strep

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peptidoglycans, capsules, hydrolytic enzymes

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Test for group b strep

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camp test. The CAMP test is a test to identify Group B β-streptococci[1][2] based on their formation of a substance (CAMP factor[3]) that enlarges the area of hemolysis formed by β-hemolysin from Staphylococcus aureus

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Strepococcus pnemoniae

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Alpha hemo, more invasive than toxigenic, capsules (very determinant of virulence).

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Infections caused by strepococcus pneumoniae

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otitis media, pnemonia, pepticemia and meningitis.

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Pre-disposing factors for stretpoc pneumoniae infections

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Viral infection, cardiac failure, alcoholism, anything that interferes with the cough reflec and epiglotall reflex.

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treatment of strepococcus pneumoniae

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PCN the best or immunization. Streptomycin works as well.

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Enterobacteriaceae

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short Gram Neg Rods. Ferments glucosewith acid with or w/o gas. Faculative (can use oxygen but can switch to fermentation for atp prd) and non spore forming. All have outer membrane and LPS. Some have capsule, flagella and pili.

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Examples of enterobacteriaceae

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E coli, salmonella (cause mild to severe infections), Klebsiella (pneumonia), proteus.

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Determinant of enterobacteriaceae pathogenicity

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1. endotoxin (lipid a)
2. enterotoxin and cytotoxins
3.invasiveness

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Dx caused by enterbacteriaceae

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Gastroenteritis, septicemia, enteric fever,pneumonia, UTI

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How is Bacturcult is used for detection of UTI

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Test for UTI infection and classification. Test for number of colonies if over 25 you are infected. Then color can determine wheather there is an inc in urea or lactose. Phenol red will turn pink(urea) as pH inc and yellow as pH dec (lactose).

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Escherichia Coli virulence factors

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Adhesins, pili, toxins such as (heat labile,heat stable, hemolysin, and shiga-like toxins).

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Shiga-like toxins

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interfere with protein synthesis and this will cause diarrhea.

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Hospital acquired UTI are caused by which bacterias?

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E.coli, proteus. and pseudomonas aerugonosa (very opportunistic)

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community acquired UTI caused by which bacterias

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E coli, Klebsiella, and proteus.

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Enterotoxigenic E.Coli (ETEC)

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prd more of a chloera like toxin which will produce watery diarrhea. INtestinal dx, produces two types of toxins LT & ST.

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ETEC produces two types of toxins

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LT-influences activity of adenyl cyclase (similar to the chloera toxin)
ST-affects guanyl cyclase

Keep cAMP levels high.both interfere with ion uptake by cells. conc of ions in interstitial tract incs. watery diarrhea.

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enterohemorrhagic E.coli (EHEC)

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More severe form of dx. Can cause uncomplicated diarrhea or severe diarrhea (shiga). Can also cause hemorrhagic colitis with severe abdominal pain and bloody diah.

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Severe complications of EHEC

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Hemolytic uremic syndrome, glomerular cells can be destroyed, hemolytic anemia/acute renal failure. young children are most susceptible.

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community acquired UTI caused by which bacterias

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E coli, Klebsiella, and proteus.

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Enterotoxigenic E.Coli (ETEC)

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prd more of a chloera like toxin which will produce watery diarrhea. INtestinal dx, produces two types of toxins LT & ST.

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ETEC produces two types of toxins

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LT-influences activity of adenyl cyclase (similar to the chloera toxin)
ST-affects guanyl cyclase

Keep cAMP levels high.both interfere with ion uptake by cells. conc of ions in interstitial tract incs. watery diarrhea.

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enterohemorrhagic E.coli (EHEC)

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More severe form of dx. Can cause uncomplicated diarrhea or severe diarrhea (shiga). Can also cause hemorrhagic colitis with severe abdominal pain and bloody diah.

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Severe complications of EHEC

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Hemolytic uremic syndrome, glomerular cells can be destroyed, hemolytic anemia/acute renal failure. young children are most susceptible.

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Shigella

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intestinal bacteria transmitted via fecal-oral route. Humans are the source of the bacteria and the infectious dose is low. intestinal dx will result and is severe but usually localized to the intestines. If becomes systemic you will ses septicemia.

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Shigella Dx

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Bacteria enters the small intestines, multiplies and travels to the terminal ileum/colon. Bacterai attaches to and invades the M-folds of the peyers patches.

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How can shigella spread?

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1. cell to cell spread
2. escape from vacuoles and multiply in cytoplasm.

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Shigella dysenteriae toxin

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produces an exotoxin. A-B type exotoxin. Stops protein synthesis!!! Loss of protein synthesis leads to loss of tissue which leads to blood in the stool.

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Progression of dx from shigella

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intiallu profuse and watery diarrhea but then lower abdominal cramps (indicative of blood loss). Diarrhea containing pus, blood, and colonic infection.

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Pathogenesis of bacteria transmitted by the enteric route

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1.mucosal adherence
2. mucosal invasion
3. mucosal translocation

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Mucosal adherence

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bacteria attaches to the surface and produces toxin. No entry into tissue is required, no invasion of the mucosal layer. Water diarrhea without blood or pus. V.Cholera is an example.

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Mucosal invasion

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cell or the submucosal area are invaded. Observable lesion, diarrhea with blood and/or pus. E.COLI and Shigella.

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Muscosal translocation

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Passage through the system. Spread throughout the body (sometimes via macrophages). Generalized symptoms like fever, shock but not GI. Salmonella typhi.

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Methods used to detect the presence of the enterotoxin

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1.Rabbit illeal loop test
2.infant mouse lethality
3.enzymatic test

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septicemia/sepsis

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salmonella bacteria, fever, shock,lesions in kidneys and lungs, GI symptoms minimal. The bacteria in this disease leave the intestines and go into other tissue. young and old at higher risk.

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Enteric/Typhoid fever

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From Salmonella, the most severe form of infection. Invade intestinal tract and penetrates the intestinal wall to get to lymph nodes. Removed by phagocytes but instead of dying in the cell they multiply and re-enter blood stream. Can also re-enter intestinal tract.

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How does salmonella resist being killed by the phagocyte?

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Antioxidant molecules

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How to treat enteric fever?

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Chloramphenicol

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Klebsiella pneumoniae

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in the intestines of animals, causes UTI and 1-5% of pneumoniae in USA. usually in males who are alcoholics or diabetic. Capsules are the main virulence factors!

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proteus

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can cause UTI, produce urease which breaks down urea into ammonia. Ammonia will raise the pH of the environment and favor proteus growth. Also the high pH can percipt calcium and magnesium salts.

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Yersinia Pestis

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Always a bacteria. Plague. Found in rodent communities. Can grow in many temperatures.

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3 Clinical forms of Y.Pestis

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1.Bubonic-reginal lymph node become infected (usually in groin) Buboes form, fever, pain in limbs.
2. Septicemic-occurs if the infection is not contained in the regional lymph nodes can spread to lung, livers.
3.Pneumonic- infection of the lungs, spread by aerosols, rapid spread and deadly.