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104 Cards in this Set
- Front
- Back
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Organization and classification
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1. Bacteria
2. Fungi 3. Viruses 4. Parasites, including protozoa and multicellular organisms 5. Means of separation |
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Distinguishing charactersitics of organisms
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1. Size Viruses<bacreria<fungi<parasites.
2. Genetic structure: DNA, RNA, or both. Viruses only have 1 or the other, higher organisms have both; DNA in baceria is usualy circular |
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Infection
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1. The growth of a microorganism in the host
2. the term infectious disease is used to indicate disease produced by a pathogen in the host. |
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pathogen
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A microrganism capable of producing disease/infection in a host.
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Virulence
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A measure of the degree of pathogenicity of a microorganism
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Normal flora (indigenous flora)
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1. Organism present on body surfaces and lumens (skin, mucous membranes, intestinal tract, etc) that do not normally cause disease at that site: Most body sites other than deep tissue have bacteria.
2. Disease is often cause by bacteria from our normal flora when some disruption in normal barriers occurs. |
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Opportunistic infections
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Caused by organisms with low virulece and require abnormal and predisposing factors such as immunosuppression, HIV infection, transplantation, or diabetes.
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Carrier state
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Being colonized. Presence of a pathogen, not causing sympthoms. may be a postinfectious state after elimination of symptoms of an infection. Temporary or indefinite.
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Infection vs colonization
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Infection indicates disease
Colonization: the onset of organism present as asymptomatic infection and may be the first step in development of infection. |
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Gram stain, helpful features
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1. Separation of bacteria into Gram Positive and Negative
2. Form of individual cell: cocci, rods or bacilli, spiral, bipolar, branching, lancet, comma, pleomorphic, coccobacilli, diplococci, fusiform. 3. Grouping of cells: clusters, pairs, chains, pallisades, chinese letters, cords, tetrads, octads. 4. Anatomic features of cells: spores, capsules, motility, beading hyphae, budding, flagella Relationships: extracellular, intracellular, adhering, epithelial, neutrophils |
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Modes of transmission
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1. Personal spread: aerosols, respiratory droplets, direct contact, body fluids, sexually.
2. Iatrogenic: hands, instruments 3. The environment: water, food, soil, etc. 4. Animals 5. Insects: mosquitoes, fleas, tick, flies. |
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steps infection
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1. attachment (organism to individual)
2. Entry 3. Survival and multiplication 4. Entry to target tissue 5. Productionof disease in target tissue 6. Retransmission-ability to transmit |
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Manifestations of Infection:
history items |
1 Exposure
2 Predisposing factors 3 Prior opportunity for prevention (immunization) 4 General symptoms: fever, sweating, chills, rigors, myalgias, arthralgias, fatigue, anorexia. 5 Organ specific symptoms |
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Manifestation of Infection:
Physical examination items |
1. Vital signs (abnormalities)
2. Appearance: toxicity 3. Organ specific signs |
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Manifestations of infection:
Lab findings |
1 WBC count
2. sedimentation rate (elevated) 3. C reactive protein 4. elevated platelet count 5.Elevated LDH 6. Organ specific abnomarmalites 7. Gram stain results 8. Culture results 9. Serologies |
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Fever: methods of measurement
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1. Old fashioned mercury thermometers (most accurate but not safe)
2. Digital thermometers 3. Site ear<oral<rectal DONT do axilary |
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Fever: General concepts
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1. Normal Range: 36-37 or 97-99
2. Normal diurnal variation, highest 4-8pm 3. Significan elevation 38.5 or 101 Dangerous range <94, >105 |
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Fever: Patterns
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1. Intermitent
2. sustained 3. Relapsing 4. temp-pulse disparity |
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Fever: attenated response
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1. Newborns
2. Elderly 3. Renal failure 4. Steroid use 5. Atypyretics |
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Penicillin resistant pneunococcus
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a.drug released in 1940
b. first resistant isolates 199 in New Guinea 1976 in S. Africa. c. 1975-85 became widespread in spain and E. Europe d. Recently spread to UK, USA and far East |
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Methicillin
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a. No resistance for two decades
b. Mec resistance gene present in many counties for a decade before spreading thorughout US c. Molecular analysis suggests one or a few mec genes have seeded resistance throughout an entire country |
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3rd generation cephalosporins
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a. Use began by 1980
b. Resistance not seen in enteric bacteria until 1985 (Germany) c. Each isolate had new b-lactamase associated with plasmid d. New genes were derivatives of earlier B-lactamase genes and enzyme hydrolyses old and new antibiotics |
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VANCOMYCIN
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a. no resistance for two decades
b. first isolagtes in Europe found on transferable elements c. Spread widely throughout world |
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Delayed emergence/wide dessemination of antimicrobial resistance
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a. gentamicin
b. resistance appeared five years after widespread introduction c. spread rapidly d. single plasmid spread resistance to many species of bacteria e. single resistance plasmid appeared suddenly in many hospitals and in many countries. |
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Emergence of Resistance Genes
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a. Baceria from patients prior to 1940 had no resistance genes
b. Resistance genes did not appear until antibiotics were used for decades c. The first strains of a species found resistant to an agent often have the same new resistance gene d. other resistance genes come later and different genes presominate in different geographical regions. e. More than 100 resistance genes have been described |
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Mutation
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1. at high frequency in all organisms due to misincorporation of nucleotides.
2. repair mechanisms correct most missmatched pairs 3. Additional specialized mechanism of DNA repair 4. Net rates of mutation ae approximately 1 per 10^7-^8 incorporated nucleotide |
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CONJUGATION
EXCHANGE OF GENETIC MATERIAL VIA DIRECT CELL TO CELL CONTACT |
a. Plasmids or whole chromosomes can be mobilized
b. Eschange usually occurs through tube like structures (pilus) c. exchange might involved pheromone induced co-aggregation (enterococcus faecalis) d. Efficiency of exchange may be very high |
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CONJUGATION
COJUGATIVE PLASMIDS |
a. Express TRA (trasfer) genes which encode proteins for pilus, plasmid binding and nicking enzyme, and several other transfer facilitaiton proteins.
b. Transferred material is single stranded c. F plasmid (fertility) in gram negative bacteria d. Transfer of plasmid form or transfer of integrated plasmid (Hfr cells) |
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CONJUGATION
R (RESISTANCE) PLASMIDS |
a. Generally conjugative
b. Include genes encoding anti-microbial resistance (often multiple genes) c. Often associated with transposon elements |
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CONJUGATION
HOST RANGE |
a. Plasmid replication and conjugation often limited to closly related bacteria.
b. Broad Host Range plasmids can replicate in and conjugate among diverse bacteria |
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CONJUGATION
Clinical Consequences |
a. Primary mechanism for exchange of genetic material among diverse bacteria
b. Rapid spread of mono and multi drug resistance |
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TRANSPOSITION
TRANSPOSABLE GENETIC ELEMENTS (TRANSPOSONS) |
Pieces of DNA that can insert into different, unrelated sies on bacterial chromosomes or plasmids.
a. insertion catalysed by transposase b. ends of transposon contain inverted repeats of DNA-target for transposase c. Insertion sequences-DNA encode only transposase d. Compound Transposon: mobile gene elem (encoding anti-microbial resistance) e. Host range may be narrow or broad |
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TRANSPOSITION
CLINICAL CONSEQUENCE |
a. Recombination independant transfer of resistance genes among unrelated plasmids or chromosomes
b. Remodeling og bacterial chromosomes and plasmids c. Source of spontaneous insertion mutations in bacteria |
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Transduction
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Exchange of genetic material via bacterophages (bacteria infecting viruses)
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Transduction: Bacterophages
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1. lytic phages: lysis of host
2. Temperate phages: integration of phage nucleic acid into bacterial genome 3. Generalized transducing phages: host and viral nucleic acid packaged during lysis. Facilitates cell to cell chromosome transfer. Plasmid readily transduced 4. specialized transducing phages: Viral and specific host nucleic acid packaged during lysis. limited cell to cell chromosome transfer |
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Transduction: Clinical consequence
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1. Rapid exchange of genetic material including plasmids among related bacteria
2. Facilitates spread of genes encoding drug resistance, toxins, etc. |
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Transformation
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1. Uptake of free DNA from surrounding environment (competent cells)
2. Great variation in efficiency (influenza very competent) 3. Clinical consequence: exchange of genetic material among distantly related organisms - broad host range. |
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Tools for molecular epidemiology
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1. Plasmid typing
2. Pulse field gel electrophoresis 3. Sequencing |
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STAPHYLOCOCCI
GENERAL CHARACTERISTICS |
a. Gram positive cocci in clusters
b. Catalase postive c. Cuagulase positive (S. aureus) and negative (many, S. epidermidis) |
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STAPHYLOCOCCI
multiple enzymes |
1. cuagulase: clot plasma
2. Alpha, beta, gamma hemolysins: lyses human red blood cells in lab. 3. Panton-Valentine Leukocidin (PVL): Hot topic a newly recognized toxin associated with more serious skin and soft tissue infections. 5. Enterotoxin: 5 product of S. aureus eg food poisoning 6. Protein A: binds to IgG 7. Other |
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STAPHILOCOCCI
Clinical Infectins |
1. Asymptomatic carriage especially on skin and anterior nares.
2. Superficial skin infection: folliculitis, abscesses, furuncles, carbuncles. 3. Foreign body infections 4. Soft tissue infections: cellulitis, fasciitis 5. Osteomyelitis 6. Bacteremia 7. Endocarditis 8. Food poisoning 9. Toxic Shock Syndrome 10. Device associated infections (iv and other catheres prostheses) To have infection with a CNS, a foreign body is usually required. |
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STAPHILOCOCCI
Clinical Manifestations of staphylococci |
3 Categories: Suppurative, toxin mediated, and device related.
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STAPHILOCOCCI
Suppurative Infection |
Organism leads to an inflamatory response, the site is invaded by white blood cells, and PUS is procude. Toxin mediated infections are the resul the tosins produced by staph that lead to a tussue response
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STAPHILOCOCCI
Predisposing Factors to Infection |
1. Suppurative infections are more likely to occur when any forein body (sutures, gauze, bandages, IV catheters, artificial joints, bone stabilizing hardware, artificial graft material, etc.) is present.
2. Breaks in the skin, invasive procedures, and devices inserted through intact skin all predispose to infection. |
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STAPHILOCOCCI
Laboratory conditions |
1. Gram stain helpful
2. Grows readily on lab media 3. Catalase and cuagulase primary test ETC |
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STAPHILOCOCCI
Superficila culture results |
Common skin flora.
Staph aureus more likely to cause disease than CNS; but either can be colonizing the surface rather than causing infection; growth of the same organism from multiple cultures is more likely to be real. |
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STREPTOCOCCI
General characteristics |
a. Gram positive cocci in chains or pairs
b. Grow best in media suppemented with blood c. Catalase negative d. Categorized by hemolysis pattern on sheep blood agar: alpha-partial or greenish heolysis, beta-complete hemlysis, gamma- no hemolysis. e. Beta strep also categorized by Lancefield groups as A,B,C, D, F,G. f. Surface structure of Group A strep very antigenic |
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Group A Strep (streptococcus pyrogenes)
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a. Causes purulent infections
b. Beta hemolytic: 2 hemolysins, Streptolysin S and Streptolysin O |
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STREPTOCOCCI
Exotoxins and enzymes that cause tissue distruction and/or shock like symptoms |
1. The M Protein: The major virulent factor, variable from strain to strain and allows subtyping; helps resist phagocytosis; antibodies agains M protein confer type specific resistance.
2. Pyrogenic exotoxins A, B, C... produce external effects including the rash of scarlet fever d. Others: streptokinase, hyaluronidase, dexoxyribunocleases, C5 alpha peptidase. |
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STREPTOCOCCI
Diseases |
1. Pharyngitis and tonsillitis: diagnose with strep screens and throat culture, complications: otitis, rheumatic fever and glomerolunephritis
2. Skin infections: impertigo, erysipelas, cellulitis, fasciitis, post-op wound infection, GN Scarlet fever: pharyngitis + strawberry tongue, rash 4. Toxic Shock-like syndrome: shock, renal failure, rash, respiratory failure. 5. RF: carditis, polyarthritis, chorea, erythema marginatum 6. GN edema, hypertension, hematuria, proteinuria RF and GN non suppurative complications 2. |
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STREPTOCOCCI
Diagnosis |
1. rapid strep screen on throats: specific, not sensitive
2. culture on blood agar 3. ASO antiDNAse B, other titers may help demonstrate recent infection |
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STREPTOCOCCI
Group B (streptococcus agalactiae) |
a. frequently colonizes female genital trackand gi tract
b. IMPORTANT CAUSE OF NEONATAL SEPSIS AND MENINGITIS (1-3/1000 live births, mortality 30-60%) c. Post-surgical gym infections. d. Infections in the elderly: uti, bacteremia, pneumonia, skin, wound infections. e. Automatic screening of all women at 35-37 weeks of gestation recomended. |
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STREPTOCOCCI
Group C,D,F,G |
a. Can cause purulent infections like group A
b. No clear association with RF or GN c. Food borne outbreaks of pharyngitis with C and G d. Bacterimia with Group D (streptococcus bovis) associated with colon cancer. e. Group F includes Streptococcus milleri, usually part of the viridans group that is associated with aggressive tissue abscesses. |
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Streptococcus Pneumoniae
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a. usually appears as a diplococci
b. Alpha hemolytic f. diseases: pneumonia, otitis, sinusitis, meningitis, bacteremia, peritonitis, septic arthritis |
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Viridians group Streptococci
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a. Alpha or nonhemolytic
b. multiple species and classification schemes c. common part of upper respiratory flora d. Disease: endocarditis, dental disease e. common contaminats in cultures. |
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ENTEROCOCCUS
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a. Formely considered Group D streptococci, now separate
b. Common part in gi tract flora b. may be non alpha or beta hemolytic d diseases: bacteremia, uti, wound, and soft tissue infections, endocarditis. e. IMPORTANT AS NOSOCOMIAL PATHOGENS f. VRE: VANCOMYCIN RESISTANT ENTEROCOCCI, also resistant to all other available antibiotics, associated with nosocomial outbreaks. |
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Aerobic Gram-POSITIVE bacilli
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As a group, these organisms lie everywhere in the environment (and or people) so they are often grown in cultures. They seldom cause disease.
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Aerobic Gram-POSITIVE bacilli
a. Listeria monocytogenes |
1. Colonizes many animals and humans,pathogen when isolated from patients
2. Short, gram positive rods, sometimes in pairs may look like CORYBACTERIA or STREP 3. Significance: Bacterimia and MENINGITIS IN NEWBORNS LAB DIAGNOSIS: culture of blood, CSF. Should see small zone of beta-hemolysis on sheep blood agar. Catalase + tumbling |
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Aerobic Gram-POSITIVE bacilli
CORYNEBACTERIUM species |
a. Present in large numbers on SKIN as NORMAL FLORA
b. Small pleomorphic gram-positive rods forming PALIDADES or "Chinese Characters" c. Commonly referred to as diphtheroids d. Significance: endocarditis, C. jeikeium causes lymphadenitis, absceses,meningitis etc; c. diphteriae. |
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DIPHTHERIA - corynebacterium diphtheriae
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1. childhood immunization protective
2. Pharyngitis with leatherly membrane with sourrounding edema. Exotoxin that affects predominantely myocardium and peripheral nervous system. Death by asphyxiation or myocarditis. |
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DIPHTHERIA - corynebacterium diphtheriae DIAGNOSIS
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Initially clinical. Therapy must be started immediately.
Confirmatiory diagnosis: throat culture on special laboratory media Lab must be notified of diphtheria suspected Lab diagnosis: methylene blue stain shows metacrhomatic granules; culture shows growth on Loeffler or Tinsdale agar |
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AEROBIC GRAM POSITIVE BACILLI
Erysipelotrix rhusiopathie |
1. colonizes domestic animals and causes infections in humans, but rarely in US.
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AEROBIC GRAM POSITIVE BACILLI
Bacillus species |
1. everywhere in the environment, often contaminate cultures
2. Form spores, unique among aerobic gram positive rods B. anthracis cause anthrax B. cereus causes food poisoning related to undercooked rice. |
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AEROBIC GRAM POSITIVE BACILLI
Lactobacillus species |
Normal flora in gi and genital tract. Ingredient in yogurt.
Virtually all protective |
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ANAEROBIC GRAM-POSITIVE BACILLI
Clostridium |
1. Common normal flora of people, animals, and soil
Clostridium perfringens (gas gangrene- rapid and progresive infection, rapid death) Food poisoning- sudden onset of nausea, vomiting, ab pain within a few hours on ingestion. Clostridium tetani- spasms and stifness |
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AEROBIC GRAM POSITIVE BACILLI
Clostridium botulinum |
1. Common soil organism
2. Type A found most often west of Mississippi, Type B most often east of the Mississippi, type E most often around bodies of water. |
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AEROBIC GRAM POSITIVE BACILLI
Clostridium difficile |
1. Most common in the USA. well recognized association with antibiotic associated pseudomembranous colitis.
Patients receiving antibiotics develop fever |
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AEROBIC GRAM POSITIVE BACILLI
Actinomycetes |
Branching gram positive organisms
Morphology led to these bacteria being classified with fungi in the past: Nocardia Actinomyces |
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ENTEROBACTERIACEAE
Morphology |
1. Gram-negative bacilli
2. Large organisms with paralled sides and rounded ends 3. Motile strains have peritrichous flagella 4. Many strains have surface pili 5. Some species are encapsulated |
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ENTEROBACTERIACEAE
Growth |
1. Grow readily on simple media after 12 to 18 hours incubation
2. Rapid growth occurs under aerobic and anaerobic conditions |
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ENTEROBACTERIACEAE
Antigenic structure |
1. O antigen (somatic) cell wall lipopolysaccharide, LPS (heat stable)
2. K antigen cell surface polysaccharide antigens (heat labile) 3. H antigen flagellar proteins (heat labile). 4. Sertyping systems for classification of these organisms have been established based upon these antigens. |
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ENTEROBACTERIACEAE
Criteria for classification to species level |
All share biochem charact:
a. Ferment glucose b. Reduce nitrates to nitrites c. Oxidase negative |
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ENTEROBACTERIACEAE
Rapid fermentation of lactose |
Pink colonies on MacConkey agar is useful for screening:
E. Coli, Klebsiella, Enterobacter (pink) |
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ENTEROBACTERIACEAE
toxins |
Endotoxins:Released when cell wall disrupted
Specific effects during infection include fever, leukopenia, activation of blood coagulation factors Enterotoxins: Produced by some species and are important in the pathogenesis of diarrheal disease |
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ENTEROBACTERIACEAE
Habitat |
1. Loger GI of animals nad humans
2. Survive readily in nature- free living in WATER and minimal energy sources are available. 3. Hospitalized patients |
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ENTEROBACTERIACEAE
Diseases |
1. UTI
2. Diarrhea GI 3. Meningitis (elderly, neonates, neurosurgical patients) 4. Bacteremia 5. Pneumonia 6. Wounds and abscesses |
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ENTEROBACTERIACEAE
Escherischia Coli |
a. Most commonly enocuntered enteric rod in the colon
C. Lactose fermenter (pink colonies in MacConkey) Beta hemolytic Most common cause of UTI Meningitis |
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ENTEROBACTERIACEAE
Klebsiella |
K. Pneumonia and K. Oxytoca are the most important species)
Lactose fermenter Second most common second cause of UTI Pneumnia |
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ENTEROBACTERIACEAE
Enterobacter |
3rd lactose fermenter
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ENTEROBACTERIACEAE
Serratia |
Red pigment (marker organism in 1940's)
opportunistic pathogen |
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ENTEROBACTERIACEAE
Citrobacter |
Biochemically similar to Salmonella
causes neonatal meningitis and bacteremia |
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ENTEROBACTERIACEAE
Proteous |
3rd most common
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ENTEROBACTERIACEAE
Enterotoxigenic E. coli (ETEC) |
1. important cause of travelers diarrhea
contaminated food and water Clinical: mild: minor disconfort, no fever, watery diarrhea, severy cholera like illness nothing really invasive |
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ENTEROBACTERIACEAE
Enterohemorragic E. Coli (EHEC) |
a. Now called Shiga-like toxin producing E. coli (E. coli 0157:H7) boody diarrhea - fast food restaurants
b. Contaminated food- beef, unpasteurized milk, apple cider c. small inoculum d. Toxin damage endothelial cells in GI tract and renal glomeruli e. incubation 3-8 days f. non-specific watery diarrhea, hemorrhagic colitis, cramps, bloody stool. Hemolytic uremic syndrome. G. Antibodies not recomended. Supportive care dialysis, prevention |
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ENTEROBACTERIACEAE
Shigella |
never a comensal in the human intestinal tract
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ENTEROBACTERIACEAE
Shigella |
4 species. S. Dysenteriae (shiga bacillus) associated with high mortality.
Invaseive organism-colonic mucosa (attack M cells) Causes hemolytic uremic syndrome. Dysenterie: ab cramps, tenesmus-painful to pass stools S. sonnei diarrhea in the US (inviasive) |
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ENTEROBACTERIACEAE
Salmonella |
Disease syndrome:
1. Gastroenteritis: improper food handling. Pultry products, summer fall peak, S. typhimurium, S. enterifidis major cause of disease; exotic reptile pets associated with infection Manifestation 24-48 hrs "food poisoning" Apicillin, trimethoprim/sulfamethoxazole, quinolones, third generation cephalosporins |
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ENTEROBACTERIACEAE
Salmonella typhi |
Thyohid fever
1. significant morbidity and mortality in the world S. typhi kills M cells Incubation period 14 days Faint rash (rose spots) Fever persisant for weeks CONSTIPATION Intestinal perforation. ABs effective: chloraphenicol, mpicillin, trimethoprim/sulfamethoxazole, ceftriaxone, quinolones vaccine! |
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ENTEROBACTERIACEAE
Yersenia |
Y. Pestis- plague
Y. enterocolica- acute mesenteric lymphadenitis (present like appencicitis) Y. Pseudotubercolosis- acute mesenteric lymphadenitis. |
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Vibrio cholerae
Agent |
1. short slightly curved Gram- negative rod
2. Single polar flagellum 3. stool characterized as rice water |
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Vibrio cholerae
Pathogenesis |
1. enterotoxin produced-responsable for the bowel wall
2. non-invasive 3. very little intestinal mucosal change 4. Profound fluid loss |
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Vivrio cholerae
disease |
incubation several hours to 5 days
Profound watery diarrhea mucus in stool-rice water Treatment- fluid therapy. tetracycline drug of choice with chloramphenicol or sulfa-trimethoprim |
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HALOPHILIC (SEA WATER) VIBRIOS
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A. Vibrio parahemolyticus
B. Vibrio vulnificus |
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CAMPYLOBACTER AND HELICOBACTER
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Facultative
gram negative 42 degree incubation selective media, extended incubation time |
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Epidemiology of enteritis
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a. contaminated food and water
b. animal reservoirs include fowl, cattle, swine, sheep, dogs, cats, etc. c. 3rd world frequency up tp 30%. Most common bacterial cause of diarrhea in the US |
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campilobacter and helicobacter
Clinical Disease: |
a. Rapid onset of fever, other constitutional symptoms, diarrhea usually w/in one day of ab pain and fever
b. ab pain specially in those w/fever and anorexia c. relapsing episodes d. spontaneous organism clearace w/in 3-6 weeks |
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Helicobacter Pylori
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a. almost universal. most individuals exposed in childhood.
b. strong associated as caused pf several gastric conditions c. looks like campylobacter d. strong urease activity e. gastritis F. PEPTIC ULCER found in association w/ PDU 90% of duodenal ulcers, 50-70% of gastric ulcers |
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Pathologic processes generally present to account for infecion of anaerobes
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1. compromised vascular supply
2. Trauma 3. Tissue distruction 4. Antecedent infections resulting in necrosis |
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Major anaerobic infection syndromes:
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a. head and neck. eg brain abscess, otitis, chronic sinusitis
b. Pulmunary: empyema (out) lung abscess (in) c. Intraabdominal: peritonitis and abscess, liver abscess. d. OB-Gyn e. Skin and soft tissue |
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General clinical clues to anaerobic infection
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a. infection contiguos to mucosal surfaces
b. foul smell c. severe necrosis with fasciitis, abscesses, ang grangrene. d. gas in tissue e. gram-stain appearance of multiple forms |
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Anaerobes:
Bacteroides |
associated with anaerobic infections in humans
developing resistance to abs |
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anaerobes:
fusobacterium species |
6 species in man, most often necrophorum, and nucleatum
common infections occur primarily in head and neck |
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anaerobes:
anaerobic cocci |
Most Peptococcus have now been reclassified as Peptostreptococcuss-brain abscesses most common
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anaerobes:
lab methods |
some infections predictable in nature.
no UTI or meningitis Collection: needle and syringe aspirate og abscesses (medium of recolection); biopses of normal sterile tissues. |
