Bakterier (bas: A Brauner) Flashcards
Vad finns det för viktiga ... G+ kocker G- kocker G+ stavar G- stavar Speciella bakterier
Vilka är aeroba/anaeroba?
AEROBER OM EJ ANNAT ANGETT G+ KOCKER * stafylokocker * streptokocker * enterokocker ** Anaeroba: anaeroba G+ kocker (samlingsnamn - typas ofta inte vidare, finns i abscesser)
G- KOCKER
- Neisseria
- Moraxella
G+ STAVAR
- corynebakterier
- Listeria monocytogenes
- Anaeroba: Clostridium pefringens, C difficile, C tetani, Propionibacterium acnes, Laktobaciller
G- STAVAR
- enterobakterier
- vibrioner
- Pseudomonas
- Stenotrophomonas maltophilia
- Acinetobacter
- Campylobacter jejuni
- Helicobacter pylori
- LV-bakterier: HI, Bordetella pertussis, Legionella
- Anaeroba: Bacteroides fragilis
SPECIELLA BAKTERIER
- SPIROKETER: Treponema pallidum, Borrelia burgdorferi
- CHLAMYDIA: C trachomatis, Chlamydophila pneumoniae
- MYKOPLASMA O UREAPLASMA: M genitalium, pneumoniae, Ureaplasma genitalium
- MYKOBAKTERIER: Mycobacterium tuberculosis
STAFYLOKOCKER
Vilka viktiga finns?
G+/G-, aeroba/anaeroba
Typer av infektioner?
Under the microscope, they appear round (cocci), and form in grape-like clusters.
S AUREUS G+, aerob
- sår, sepsis, matförgiftning, toxic shock syndrome
KNS G+, aeroba
- lågvirulenta men ofta AB-resistenta
- S EPIDERMIDIS
- vanligaste i normalfloran, men kan ge infektioner
- S LUGDUNENSIS
- mer virulent än andra KNS
S SAPROPHYTICUS G+, aerob
- UVI hos unga kvinnor
STREPTOKOCKER
Vilka viktiga finns?
G+/G-, aeroba/anaeroba
Typer av infektioner?
Vad är skillnaden mellan α- och β-strep?
Strep växer i regel i par eller kedjor.
Alla är G+, aeroba
S PENUMONIAE
- pneumoni, meningit, otit, sinuit, sepsis
S PYOGENES (β-STREP GRUPP A = GAS) - virulent; svalginf, scarlatina, svinkoppor, rosfeber, matförgiftning, sårinf, sepsis, myosin mm
β-STREP GRUPP C, GRUPP G
- liknar A, men mindre virulenta
S AGALACTIAE (tillhör S GRUPP B - i regel β-hemolytiska) - neonatal sepsis (ger ofta missfall, dödar 10-20 barn/år i SE, meningit
α-STREP
- munhåla (S viridans är ett samlingsnamn för ett stort antal α- o icke-hemolytiska strep, normalflora i mun o svalg, vanlig orsak till karies o endokardit, kan ge abscesser o sepsis) tarm, endokardit
Arterna grupperas efter flera olika system, bland annat i grupper från A till W beroende på serotyp (något förenklat kolhydratsorter i de delar av bakterien som kroppen bildar antikroppar mot) och efter arternas hemolytiska egenskaper. Man talar om alfa- respektive betahemolytiska streptokocker. Betahemolytiska arter hemolyserar fullständigt, alfahemolytiska arter endast ofullständigt.
HEMOLYS
Vad kan orsaka hemolys i kroppen?
Vilka bakterier kan orsaka hemolys?
Andra orsaker till hemolys?
Hemolysis inside the body can be caused by a large number of medical conditions, including many Gram-positive bacteria (e.g., Streptococcus, Enterococcus, and Staphylococcus), some parasites (e.g., Plasmodium), some autoimmune disorders (e.g., drug-induced hemolytic anemia), some genetic disorders (e.g., Sickle-cell disease or G6PD deficiency), or blood with too low a solute concentration (hypotonic to cells).
Hemolysis can lead to hemoglobinemia due to hemoglobin released into the blood plasma.
Many species of the genus STREPTOCOCCUS cause hemolysis. Streptococcal bacteria species are classified according to their hemolytic properties. Note that these hemolytic properties do not necessarily present in vivo.
Alpha-hemolytic species, including S. pneumoniae, Streptococcus mitis, S. mutans, and S. salivarius, oxidize the iron in the hemoglobin (turning it dark green in culture).
Beta-hemolytic species, including S. pyogenes and S. agalactiae, completely rupture the red blood cells (visible as a halo in culture).
Gamma-hemolytic, or non-hemolytic, species do not cause hemolysis and rarely cause illness.
The genus ENTEROCOCCUS includes lactic acid bacteria formerly classified as gamma-hemolytic Group D in the genus streptococcus (see above), including E. faecilis (S. faecalis), E. faecium (S. faecium), E. durans (S. durans), and E. avium (S. avium).
STAPHYLOCOCCUS is another Gram-positive cocci. S. aureus, the most common cause of “staph” infections, is frequently hemolytic on blood agar.
ANDRA ORSAKER
* Because the feeding process of the Plasmodium parasites damages red blood cells, malaria is sometimes called “parasitic hemolysis” in medical literature.
- HELLP-syndrome, pre-eclampsia, eclampsia
- Hemolytic disease of the newborn is an autoimmune disease resulting from the mother’s antibodies crossing the placenta to the fetus.
- Because in vivo hemolysis destroys the red blood cells, in uncontrolled chronic or severe cases it can lead to hemolytic anemia.
- A hemolytic crisis, or hyperhemolytic crisis, is characterized by an accelerated rate of red blood cell destruction leading to anemia, jaundice, and reticulocytosis.[3] Hemolytic crises are a major concern with sickle-cell disease and G6PD deficiency.
- Paxillus Involutus (pluggskivling) ingestion can cause Hemolysis.
ENTEROKOCKER
Vilka viktiga finns?
G+/G-, aeroba/anaeroba
Typer av infektioner?
Förekommer i tarmen, lågvirulenta. Alltid resistenta mot cefalosporiner. Kan också vara resistenta mot vankomycin: VRE
E FAECALIS - UVI
E FAECIUM - UVI, ofta ampicillin-resistent
Enterococcus is a large genus of lactic acid bacteria of the phylum Firmicutes. Enterococci are Gram-positive cocci that often occur in pairs (diplococci) or short chains, and are difficult to distinguish from streptococci on physical characteristics alone.[4] Two species are common commensal organisms in the intestines of humans: E. faecalis (90–95%) and E. faecium (5–10%). Rare clusters of infections occur with other species, including E. casseliflavus, E. gallinarum, and E. raffinosus.
Enterococci are facultative anaerobic organisms, i.e., they are capable of cellular respiration in both oxygen-rich and oxygen-poor environments.[5] Though they are not capable of forming spores, enterococci are tolerant of a wide range of environmental conditions: extreme temperature (10–45 °C), pH (4.5–10.0), and high sodium chloride concentrations.[6]
Enterococci typically exhibit alpha-hemolysis on sheep’s blood agar.
Important clinical infections caused by Enterococcus include urinary tract infections, bacteremia, bacterial endocarditis, diverticulitis, and meningitis.[6][7] Sensitive strains of these bacteria can be treated with ampicillin, penicillin and vancomycin.[10] Urinary tract infections can be treated specifically with nitrofurantoin, even in cases of vancomycin resistance.[11]
From a medical standpoint, an important feature of this genus is the high level of intrinsic antibiotic resistance. Some enterococci are intrinsically resistant to β-lactam-based antibiotics (penicillins, cephalosporins, carbapenems), as well as many aminoglycosides.[7] In the last two decades, particularly virulent strains of Enterococcus that are resistant to vancomycin (vancomycin-resistant Enterococcus, or VRE) have emerged in nosocomial infections of hospitalized patients, especially in the US.[6] Other developed countries, such as the UK, have been spared this epidemic, and, in 2005, Singapore managed to halt an epidemic of VRE.[12] VRE may be treated with quinupristin/dalfopristin (Synercid) with response rates around 70%.[13] Tigecycline has also been shown to have antienterococcal activity, as has rifampicin.[citation needed]
Enterococcal meningitis is a rare complication of neurosurgery. It often requires treatment with intravenous or intrathecal vancomycin, yet it is debatable as to whether its use has any impact on outcome: the removal of any neurological devices is a crucial part of the management of these infections.[14] New epidemiological evidence has shown that enterococci are major infectious agent in chronic bacterial prostatitis.[citation needed] Enterococci are able to form biofilm in the prostate gland, making their eradication difficult.
CORYNE-BAKTERIER
Vilka viktiga finns?
G+/G-, aeroba/anaeroba
Typer av infektioner?
G+ stavar
Finns generellt som normalflora i hud, svalg
Undantag:
C DIPHTERIAE difteri
Vissa kan vara opportunistiska patogener, C jeikeium (= JK-difteroid) o några andra är extremt ab-resistenta
Vad finns det för …
* G+ stavar?
G+ stavar:
AEROBER
- Corynebakterier: C diphteriae, C jeikeium (JK-difteroid)
- Listeria monocytogenes
ANAEROBER
Clostridium (perfringens, difficile, tetani)
Proprionibacterium acnes
Lactobaciller
LISTERIA MONOCYTOGENES
G+/G-, aerob/anaerob
Typer av infektioner?
Aerob, G+ stav
Sepsis, meningit, särskilt neonatalt o hos immunsupprimerade
Alltid resistent mot cefalosporin
G- KOCKER
Vilka viktiga finns?
aeroba/anaeroba
Typer av infektioner?
NEISSERIA
- N meningitidis = meningokock
- meningit, sepsis
- N gonorrhoeae
- STD
- Apatogena neisseria-arter
- Del av normalfloran
MORAXELLA (BRANHAMELLA)
- M. catarrhalis
- LVI
Vad finns det för …
* G- stavar?
AEROBER: ENTEROBAKTERIER = ENTEROBACTERIACEAE * E coli - UVI - EHEC, ETEC, EPEC, EIEC - tarminf * Klebsiella - UVI * Enterobacter - UVI * Proteus-gruppen - UVI (P mirabilis, P vulgaris, Morganella morganii) * Citrobacter - UVI * Serratia - UVI, ofta vårdrelaterade
- Salmonella - tarminf (S typhi, S paratyphi)
- Shigella - tarminf (S dysenteriae, S flexneri, S boydii, S sonnei)
- Yersinia - tarminf
VIBRIONER
- Vibrio cholerae - tarminf, badsårsfeber
- Aeromonas - tarminf
ANDRA G- STAVAR (kan vara opportunistiska)
- Pseudomonas aeruginosa - UVI - krävs speciella ab
- Stenotrophomonas maltophilia - sår, LV - resistent mot de flesta ab
- Acinetobacter - UVI - kan ha ovanligt resistensmönster
CAMPYLOBACTER O HELICOBACTER
- Campylobacter jejuni - tarminf
- Helicobacter pylori - magsår
LUFTVÄGSBAKTERIER
- Haemophilus influenza - LVI
- Bordetella pertussis - LVI
- Legionella - LVI
ANAEROBER:
* Bacteroides fragilis - abscesser, sårinfektioner
Members of the Enterobacteriaceae are bacilli (rod-shaped), and are typically 1–5 μm in length. They typically appear as medium to large-sized grey colonies on blood agar, although some can express pigments (such as Serratia marcescens). Like other proteobacteria, enterobactericeae have Gram-negative stains,[8] and they are facultative anaerobes, fermenting sugars to produce lactic acid and various other end products. Most also reduce nitrate to nitrite, although exceptions exist.
Most members of Enterobacteriaceae have peritrichous, type I fimbriae involved in the adhesion of the bacterial cells to their hosts. Some enterobacteria produce endotoxins. Endotoxins reside in the cell wall and are released when the cell dies and the cell wall disintegrates. Some members of the Enterobacteriaceae produce endotoxins that, when released into the bloodstream following cell lysis, cause a systemic inflammatory and vasodilatory response. The most severe form of this is known as endotoxic shock, which can be rapidly fatal.
Several Enterobacteriaceae strains have been isolated which are resistant to antibiotics including carbapenems, which are often claimed as “the last line of antibiotic defense” against resistant organisms. For instance, some Klebsiella pneumoniae strains are carbapenem resistant.
KATALAS
Hur används katalas-testet?
Vilka bakterier är katalas-positiva? (-negativa?)
Vilken roll spelar katalas för bakteriell virulens?
Vad har katalas ev att göra med grått hår?
The catalase test is one of the three main tests used by microbiologists to identify species of bacteria. If the bacteria possess catalase (i.e., are catalase-positive), when a small amount of bacterial isolate is added to hydrogen peroxide, bubbles of oxygen are observed. The catalase test is done by placing a drop of hydrogen peroxide on a microscope slide. An applicator stick is touched to the colony, and the tip is then smeared onto the hydrogen peroxide drop.
If the mixture produces bubbles or froth, the organism is said to be ‘catalase-positive’. STAPHYLOCOCCI and MICROCOCCI are catalase-positive. Other catalase-positive organisms include LISTERIA, CORYNEBACTERIUM DIPHTHERIAE, BURKHOLDERIA CEPACIA, NOCARDIA, the family ENTEROBACTERIACEAE (CITROBACTER, E. COLI, ENTEROBACTER, KLEBSIELLA, SHIGELLA, YERSINIA, PROTEUS, SALMONELLA, SERRATIA), PSEUDOMONAS, MYCOBACTERIUM TUBERCULOSIS, ASPERGILLUS, CRYPTOCOCCUS, and RHODOCOCCUS EQUI.
If not, the organism is ‘catalase-negative’. STREPTOCOCCUS and ENTEROCOCCUS spp. are catalase-negative.
While the catalase test alone cannot identify a particular organism, it can aid identification when combined with other tests such as antibiotic resistance. The presence of catalase in bacterial cells depends on both the growth condition and the medium used to grow the cells.
Capillary tubes may also be used. A small sample of bacteria is collected on the end of the capillary tube, without blocking the tube, to avoid false negative results. The opposite end is then dipped into hydrogen peroxide, which is drawn into the tube through capillary action, and turned upside down, so that the bacterial points downwards. The hand holding the tube is then tapped on the bench, moving the hydrogen peroxide down until it touches the bacteria. If bubbles form on contact, this indicates a positive catalase result. This test can detect catalase-positive bacteria at concentrations above about 105 cells/mL, and is simple to use.
BACTERIAL VIRULENCE
Neutrophils and other phagocytes use peroxide to kill bacteria. The enzyme NADPH oxidase generates superoxide within the phagosome, which is converted via hydrogen peroxide to other oxidising substances like hypochlorous acid which kill phagocytosed pathogens.[49] In individuals with chronic granulomatous disease (CGD) there is a defect in producing peroxide via mutations in phagocyte oxidases such as myeloperoxidase.[50] Normal cellular metabolism will still produce a small amount of peroxide and this peroxide can be used to produce hypochlorous acid to eradicate the bacterial infection. However, if individuals with CGD are infected with catalase-positive bacteria, the bacterial catalase can destroy the excess peroxide before it can be used to produce other oxidising substances. In these individuals the pathogen survives and becomes a chronic infection. This chronic infection is typically surrounded by macrophages in an attempt to isolate the infection. This wall of macrophages surrounding a pathogen is called a granuloma. Many bacteria are catalase positive, but some are better catalase-producers than others. The mnemonic “cats Need PLACESS to Belch their Hairballs” can be used to memorise the catalase-positive bacteria: nocardia, pseudomonas, listeria, aspergillus, candida, E. coli, staphylococcus, serratia, B. cepacia and H. pylori.
GRAY HAIR
Low levels of catalase may play a role in the graying process of human hair. Hydrogen peroxide is naturally produced by the body and broken down by catalase. If catalase levels decline, hydrogen peroxide cannot be broken down so well. The hydrogen peroxide interferes with the production of melanin, the pigment that gives hair its color.
E COLI
- Vad står E för?
- G+/-, aerob/anaerob?
- Vilka är de huvudsakliga patotyperna av E coli som ger diarré, UVI?
Escherichia coli /ˌɛʃɪˈrɪkiə ˈkoʊlaɪ/
G-, fakultativt anaeroba stavar, 0,9 % av tarmfloran
Enteric E. coli (EC) are classified on the basis of serological characteristics and virulence properties. The major pathotypes of E. coli that cause diarrhea are listed below:
ETEC - enterotoxigen E coli
- diarré utan feber, binder till enterocyter i tunntarmen aha adhesiner t fimbrier, noninvasive, vanligaste orsak till barndiarré i u-länder o till turistdiarré
ETEC can produce two proteinaceous enterotoxins:
* The larger of the two proteins, LT enterotoxin, is similar to cholera toxin in structure and function.
* The smaller protein, ST enterotoxin causes cGMP accumulation in the target cells and a subsequent secretion of fluid and electrolytes into the intestinal lumen.
EPEC - enteropatogen E coli
- diarré, använder adhesinet intimin f att binda till och ta sig in i enterocyter vilket triggar inflammation o deformerar cellerna - det senare trolig orsak till diarrén; har många virulensfaktorer som liknar Shigellas.
EIEC - enteroinvasiv E coli
- ger syndrom identiskt med shigellos = profuse diarrhea and high fever
EHEC - enterohemorragisk E coli
- värsta serotypen är O157:H7 som ger blodig diarré utan feber; kan orsaka HUS (hemolytiskt-uremiskt syndrom) o akut njursvikt; binder t enterocyter mha fimbrier (ECP - E coli common pilus), är måttligt invasiv, har fag-kodat shigatoxin som kan orsaka intensiva inflammationssvar
EAEC - enteroaggregativ E coli
- har fimbrier som aggregerad vävnadskulturceller; binder till mukosan –> vattnig diarré utan feber - noninvasiv; producerar hemolysin och ett ST enterotoxin liknande ETEC
AIEC - adherent invasive E coli
- kan invadera enterocyter o replikera i dem, troligen särskilt snabbt i värdar med defekt medfött immunförsvar; associerade med Crohns sjd.
UPEC - uropathogenic E coli
Uropathogenic E. coli (UPEC) is responsible for approximately 90% of urinary tract infections (UTI) seen in individuals with ordinary anatomy.[12] In ascending infections, fecal bacteria colonize the urethra and spread up the urinary tract to the bladder as well as to the kidneys (causing pyelonephritis),[39] or the prostate in males. Because women have a shorter urethra than men, they are 14 times more likely to suffer from an ascending UTI.[12]
Uropathogenic E. coli use P fimbriae (pyelonephritis-associated pili) to bind urinary tract urothelial cells and colonize the bladder. These adhesins specifically bind D-galactose-D-galactose moieties on the P blood-group antigen of erythrocytes and uroepithelial cells.[12] Approximately 1% of the human population lacks this receptor,[citation needed] and its presence or absence dictates an individual’s susceptibility or non-susceptibility, respectively, to E. coli urinary tract infections. Uropathogenic E. coli produce alpha- and beta-hemolysins, which cause lysis of urinary tract cells.
Another virulence factor commonly present in UPEC is the Dr family of adhesins, which are particularly associated with cystitis and pregnancy-associated pyelonephritis. The Dr adhesins bind Dr blood group antigen (Dra) which is present on decay accelerating factor (DAF) on erythrocytes and other cell types. There, the Dr adhesins induce the development of long cellular extensions that wrap around the bacteria, accompanied by the activation of several signal transduction cascades, including activation of PI-3 kinase.
UPEC can evade the body’s innate immune defences (e.g. the complement system) by invading superficial umbrella cells to form intracellular bacterial communities (IBCs). They also have the ability to form K antigen, capsular polysaccharides that contribute to biofilm formation. Biofilm-producing E. coli are recalcitrant to immune factors and antibiotic therapy, and are often responsible for chronic urinary tract infections. K antigen-producing E. coli infections are commonly found in the upper urinary tract.
Descending infections, though relatively rare, occur when E. coli cells enter the upper urinary tract organs (kidneys, bladder or ureters) from the blood stream.
Most E. coli strains are harmless, but some serotypes are pathogenic and can cause serious food poisoning in humans, and are occasionally responsible for product recalls. E. coli are also responsible for a majority of cases of urinary tract infections. The harmless strains are part of the normal flora of the gut, and can benefit their hosts by producing vitamin K2, and by preventing the establishment of pathogenic bacteria within the intestine.
E. coli is expelled into the environment within fecal matter. The bacterium grows massively in fresh fecal matter under aerobic conditions for 3 days, but its numbers decline slowly afterwards.
In humans and in domestic animals, virulent strains of E. coli can cause various diseases.
In humans : gastroenteritis, urinary tract infections, and neonatal meningitis. In rarer cases, virulent strains are also responsible for hemolytic-uremic syndrome, peritonitis, mastitis, septicaemia and gram-negative pneumonia.
Intestinal mucosa-associated E. coli are observed in increased numbers in the inflammatory bowel diseases, Crohn’s disease and ulcerative colitis.[15] Invasive strains of E. coli exist in high numbers in the inflamed tissue, and the number of bacteria in the inflamed regions correlates to the severity of the bowel inflammation.[16]
Gastrointestinal infections can cause the body to develop memory T cells to attack gut microbes that are in the intestinal tract. Food poisoning can trigger an immune response to microbial gut bacteria. Some researchers suggest that it can lead to inflammatory bowel disease
PSEUDOMONAS AERUGINOSA
G+/G-, aeroba/anaeroba
Typer av infektioner? Varför anses den vara opportunist?
G- stav
Resistens f många AB
- Kan ge allvarliga sjd såsom nosokomiala infektioner såsom ventilatorassocierad pneumoni o sepsis, den vanligaste kolonisatören av medicinsk utrustning såsom kateter. Pseudomonas can be spread by equipment that gets contaminated and is not properly cleaned or on the hands of healthcare workers.
- hot tub folliculitis; since these bacteria like moist environments, such as hot tubs and swimming pools, they can cause skin rash or swimmer’s ear
- An opportunistic, nosocomial pathogen of immunocompromised individuals, P. aeruginosa typically infects the airway, urinary tract, burns, and wounds, and also causes other blood infections.
- penumoni - diffus bronkopneumoni - CF pt högrisk
- septisk chock - neutropena
- UVI - kateterisering
- GI - nekrotiserande enterokolit - prematura barn o neutropena cancerpt
- hud o mjukdelar - blödning o nekros - brännskador, sårinfektioner, otitis externa
The organism is considered opportunistic insofar as serious infection often occurs during existing diseases or conditions – most notably cystic fibrosis and traumatic burns. It is also found generally in the immunocompromised but can infect the immunocompetent as in hot tub folliculitis.
It is citrate, catalase, and oxidase positive. It is found in soil, water, skin flora, and most man-made environments throughout the world. It thrives not only in normal atmospheres, but also in low-oxygen atmospheres, thus has colonized many natural and artificial environments. It uses a wide range of organic material for food; in animals, its versatility enables the organism to infect damaged tissues or those with reduced immunity. The symptoms of such infections are generalized inflammation and sepsis. If such colonizations occur in critical body organs, such as the lungs, the urinary tract, and kidneys, the results can be fatal.[1] Because it thrives on moist surfaces, this bacterium is also found on and in medical equipment, including catheters, causing cross-infections in hospitals and clinics. It is also able to decompose hydrocarbons and has been used to break down tarballs and oil from oil spills.[2] P. aeruginosa is not extremely virulent in comparison with other major pathogenic bacterial species – for example Staphylococcus aureus and Streptococcus pyogenes – though P. aeruginosa is capable of extensive colonization, and can aggregate into enduring biofilms.
BEHANDLING
Many P. aeruginosa isolates are resistant to a large range of antibiotics and may demonstrate additional resistance after unsuccessful treatment. It should usually be possible to guide treatment according to laboratory sensitivities, rather than choosing an antibiotic empirically. If antibiotics are started empirically, then every effort should be made to obtain cultures (before administering first dose of antibiotic), and the choice of antibiotic used should be reviewed when the culture results are available.
Antibiotics that may have activity against P. aeruginosa include:
aminoglycosides (gentamicin, amikacin, tobramycin, but not kanamycin)
quinolones (ciprofloxacin, levofloxacin, but not moxifloxacin)
cephalosporins (ceftazidime, cefepime, cefoperazone, cefpirome, ceftobiprole, but not cefuroxime, cefotaxime, or ceftriaxone)
antipseudomonal penicillins: carboxypenicillins (carbenicillin and ticarcillin), and ureidopenicillins (mezlocillin, azlocillin, and piperacillin). P. aeruginosa is intrinsically resistant to all other penicillins.
carbapenems (meropenem, imipenem, doripenem, but not ertapenem)
polymyxins (polymyxin B and colistin)[52]
monobactams (aztreonam)
As fluoroquinolone is one of the few antibiotics widely effective against P. aeruginosa, in some hospitals, its use is severely restricted to avoid the development of resistant strains. On the rare occasions where infection is superficial and limited (for example, ear infections or nail infections), topical gentamicin or colistin may be used.
For pseudomonal wound infections, acetic acid with concentrations from 0.5% to 5% can be an effective bacteriostatic agent in eliminating the bacteria from the wound. Usually a sterile gauze soaked with acetic acid is placed on the wound after irrigation with normal saline. Dressing would be done once per day. Pseudomonas is usually eliminated in 90% of the cases after 10 to 14 days of treatment.
HAEMOPHILUS INFLUENZAE
BORDETELLA PERTUSSIS
LEGIONELLA
- Vad är gemensamma nämnare?
- G+/G-, aeroba/anaeroba
- Typer av infektioner?
- Aeroba G- stavar, luftvägsbakterier
HAEMOPHILUS INFLUENZAE
- fakultativt anaerob; trodde först att den var orsak till influensa, sedan kallas sjd i dagligt tal “bacterial influenza”
- opportunist: Most strains of H. influenzae are opportunistic pathogens; that is, they usually live in their host without causing disease, but cause problems only when other factors (such as a viral infection, reduced immune function or chronically inflamed tissues, e.g. from allergies) create an opportunity. They infect the host by sticking to the host cell using trimeric autotransporter adhesins.
- Naturally acquired disease caused by H. influenzae seems to occur in humans only. In infants and young children, H. influenzae type b (Hib) causes BACTEREMIA, PNEUMONIA, EPIGLOTTITIS and ACUTE BACTERIAL MENINGITIS. On occasion, it causes CELLULITIS, OSTEOMYELITIS, and INFECTIOUS ARTHRITIS. It is one cause of NEONATAL INFECTION.
Due to routine use of the Hib conjugate vaccine in the U.S. since 1990, the incidence of invasive Hib disease has decreased to 1.3/100,000 in children. However, Hib remains a major cause of LOWER RESPIRATORY TRACT INFECTIONS in infants and children in developing countries where the vaccine is not widely used. UNENCAPSULATED H. INFLUENZAE STRAINS are unaffected by the Hib vaccine and cause EAR INFECTIONS (OTITIS MEDIA), EYE INFECTIONS (CONJUNCTIVITIS), AND SINUSITIS in children, and are associated with PNEUMONIA.
- LVI
- Clinical features may include initial symptoms of an upper respiratory tract infection mimicking a viral infection, usually associated with fevers, often low-grade. This may progress to the lower respiratory tract in a few days, with features often resembling those of a wheezy bronchitis.
- Haemophilus influenzae produces beta-lactamases, and it is also able to modify its penicillin-binding proteins, so it has gained resistance to the penicillin family of antibiotics. In severe cases, cefotaxime and ceftriaxone delivered directly into the bloodstream are the elected antibiotics, and, for the less severe cases, an association of ampicillin and sulbactam, cephalosporins of the second and third generation, or fluoroquinolones are preferred. (Fluoroquinolone-resistant Haemophilus influenzae have been observed.)[15]
Macrolide antibiotics (e.g., clarithromycin) may be used in patients with a history of allergy to beta-lactam antibiotics.[citation needed] Macrolide resistance has also been observed. The serious complications of HiB are brain damage, hearing loss, and even death.
BORDETELLA PERTUSSIS
- G- aerob, kapslad, ger pertussis = kikhosta, droppsmitta, inkubation 9-10 d(6-20)
- LVI: Pertussis is an infection of the respiratory system characterized by a “whooping” sound when the person breathes in. In the US, it killed between 10,000 and 20,000 people per year before a vaccine was available.
- B. pertussis infects its host by colonizing lung epithelial cells. The bacterium contains a surface protein, filamentous haemagglutinin adhesin, which binds to the sulfatides found on cilia of epithelial cells. Once anchored, the bacterium produces tracheal cytotoxin, which stops the cilia from beating. This prevents the cilia from clearing debris from the lungs, so the body responds by sending the host into a coughing fit. These coughs expel some bacteria into the air, which are free to infect other hosts.
- The infection occurs mostly in children under the age of one when they are unimmunized, or children with faded immunity, normally around the ages 11 through 18. The signs and symptoms are similar to a common cold: runny nose, sneezing, mild cough, and low-grade fever. The patient becomes most contagious during the catarrhal stage of infection, normally two weeks after the coughing begins. It may become airborne when the person coughs, sneezes, or laughs.
LEGIONELLA
In the natural environment, Legionella lives within amoebae such as Acanthamoeba spp., Naegleria spp., and Vermamoeba vermiformis, or other protozoa such as Tetrahymena pyriformis.
Upon inhalation, the bacteria can infect alveolar macrophages, where the bacteria can replicate. This results in Legionnaires’ disease and the less severe illness Pontiac fever.
LEGIONÄRSSJUKA
- Legionnaires’ disease is a form of atypical pneumonia caused by any type of Legionella bacteria.[4] Signs and symptoms include cough, shortness of breath, high fever, muscle pains, and headaches.[3] Nausea, vomiting, and diarrhea may also occur.[1] This often begins two to ten days after exposure.
The bacterium is found naturally in fresh water.[5] It can contaminate hot water tanks, hot tubs, and cooling towers of large air conditioners.[5] It is usually spread by breathing in mist that contains the bacteria.[5] It can also occur when contaminated water is aspirated.[5] It typically does not spread directly between people and most people who are exposed do not become infected.[5] Risk factors for infection include older age, history of smoking, chronic lung disease, and poor immune function.[6] It is recommended that those with severe pneumonia and those with pneumonia and a recent travel history be tested for the disease.[11] Diagnosis is by a urinary antigen test and sputum culture.
- Treatment of Legionnaires’ disease is with antibiotics. Recommended agents include fluoroquinolones, azithromycin, or doxycycline. Hospitalization is often required. About 10% of those who are infected die.
- The length of time between exposure to the bacteria and the appearance of symptoms is generally two to ten days, but can rarely extend to as much as 20 days.[15] For the general population, among those exposed between 0.1% and 5% develop disease, while among those in hospital between 0.4% and 14% develop disease.
Those with Legionnaires’ disease usually have fever, chills, and a cough, which may be dry or may produce sputum. Almost all with Legionnaires’ experience fever, while approximately half have cough with sputum, and one third cough up blood or bloody sputum. Some also have muscle aches, headache, tiredness, loss of appetite, loss of coordination (ataxia), chest pain, or diarrhea and vomiting.[16] Up to half of those with Legionnaires’ disease have gastrointestinal symptoms, and almost half have neurological symptoms,[15] including confusion and impaired cognition.[17] “Relative bradycardia” may also be present, which is low or low-normal heart rate despite the presence of a fever.
Laboratory tests may show that kidney functions, liver functions and electrolyte levels are abnormal, which may include low sodium in the blood. Chest X-rays often show pneumonia with consolidation in the bottom portion of both lungs. It is difficult to distinguish Legionnaires’ disease from other types of pneumonia by symptoms or radiologic findings alone; other tests are required for definitive diagnosis.
Persons with Pontiac fever experience fever and muscle aches without pneumonia. They generally recover in two to five days without treatment. For Pontiac fever the time between exposure and symptoms is generally a few hours to two days.
Over 90% of cases of Legionnaires’ disease are caused by the bacteria Legionella pneumophila. Other types include L. longbeachae, L. feeleii, L. micdadei, and L. anisa.
PONTIAC FEVER is an acute, nonfatal respiratory disease caused by various species of Gram-negative bacteria in the genus Legionella. It causes a mild upper respiratory infection that resembles acute influenza. Pontiac fever resolves spontaneously and often goes undiagnosed. Both Pontiac fever and the more severe Legionnaire’s disease are caused by the same bacteria, but Pontiac fever does not include pneumonia.
LEGIONELLA PNEUMOPHILA
- G- aerob
- L. pneumophila is a facultative intracellular parasite that can invade and replicate inside amoebae in the environment, which can thus serve as a reservoir for L. pneumophila, as well as provide protection from environmental stresses, such as chlorination.
- In humans, L. pneumophila invades and replicates inside macrophages. The internalization of the bacteria can be enhanced by the presence of antibody and complement, but is not absolutely required. Internalization of the bacteria appears to occur through phagocytosis. However, L. pneumophila is also capable of infecting nonphagocytic cells through an unknown mechanism. A rare form of phagocytosis known as coiling phagocytosis has been described for L. pneumophila, but this is not dependent on the Dot/Icm secretion system and has been observed for other pathogens.[7] Once internalized, the bacteria surround themselves in a membrane-bound vacuole that does not fuse with lysosomes that would otherwise degrade the bacteria. In this protected compartment, the bacteria multiply.
- LVI
ANAEROBA BAKTERIER
- Anaeroba G+ kocker
- Anaeroba G+ stavar
- Anaeroba G- stavar
- Vilka, typ av infektioner?
FOLKHÄLSOMYNDIGHETEN:
“I rutindiagnostiken är det som regel tillräckligt att identifiera B. fragilis och Clostridium perfingens till speciesnivå. Övriga anaerober kan identifieras till presumtiv speciesnivå, t.ex. Bacteroides species, Prevotella species etc. Nedan beskrivs minimikriterier för denna rutindiagnostiska nivå.”
ANAEROBA G+ KOCKER
- samlingsnamn, ofta typas de inte vidare.
- återfinns i abscesser
- Peptococcus niger. Ovanlig i kliniskt material. Skiljer sig från peptostreptokocker genom svag katalaspositivitet och pigmentering synlig i plattmikroskop.
- Peptostreptokocker (gruppbestämning).
Grampositiva kocker. Kanamycin och vankomycinkänsliga. Katalas- och indolnegativa.
ANAEROBA G+ STAVAR
- Clostridium perfringens - tarminf, sårinf
- Clostridium difficile - tarminf
- Clostridium tetani - tetanus, sårinfektioner
- Propionibacterium acnes - tillhör normalfloran på huden
- Lactobaciller - tillhör normalfloran i vagina hos fertila kvinnor
- Actinomyces - Actinomyces spp är allmänt förekommande i munhåla hos människor och djur och utgör en signifikant komponent i dentala plaque. Möjligen tillhör de också den normala genitala bakteriefloran. De anses spela en viss roll i normalflorans skydd mot kolonisering med externa patogener.
Vissa species oftast i blandkultur har speciellt associerats med infektioner hos människa nämligen aktinomykos (A. israelii, A. gerencseriae och i mindre utsträckning A. naeslundi, A. viscosus, A. odontolyticus) och periodontit (A. viscosus och A. naeslundi). Nyligen beskrivna arter har isolerats från blod och vid UVI.
- till gruppen hör även: Eubacterium, Bifidobacterium och Mobiluncus;
ANAEROBA G- STAVAR
- Bacteroides fragilis - abscesser, sårinfektioner; kanamycin och vankomycinresistenta. Katalaspositiv. Indolnegativ. Eventuellt kan colistin och oxgalla komplettera diagnostiken.
MER OM AKTINOMYKOS
Patogenes och patofysiologi
Infektion med aktinomyceter betraktas som klassiskt endogen med spridning från munhålan till andra ställen i kroppen. De kan dock ej penetrera frisk slemhinna, varför mukosaskada är en förutsättning för infektion i underliggande vävnad och vidare spridning. Trauma eller kirurgi ligger ofta bakom en infektion. Etablerad infektion tenderar att fortsätta över anatomiska gränser.
Aktinomykos karakteriseras av kroniska granulomatösa förändringar som blir suppurerande, bildar abscesser och ger djupa fistulerande sår. Pus innehåller ofta “sulfurgranulae” som kan vara vita, gula eller bruna. Sådana bildas enbart in vivo.
A. israelii är vanligaste orsaken till aktinomykos men infektionen är oftast polymikrobiell, vilket säkert bidrar till patogenesen.
Symtom och klinisk bild
Den vanligaste lokalisationen av aktinomykos är ansikte och hals (32-48 %), abdomen (22-69 %) och thorax (15-30 %). Aktinomykos i bäckenet förekommer hos kvinnor med IUD (intrauterin kontraceptiv spiral). Bakom den thorakala formen ligger kronisk lungsjukdom, dental kirurgi, aspiration eller penetrerande trauma.
Infektionen kan börja smygande med ospecifika symtom vilka initialt misstolkas som malignitet eller annan kronisk infektion. Kronisk hosta och bröstsmärtor är mer typiska symtom. Periostit och engagemang av benvävnad bör öka misstanken. Pleura är ofta involverad. Vid klassisk thorakal aktinomykos sågs fistulering till bröstkorgen. Diagnosen sker på klinisk grund och genom påvisande av organismen i biopsimaterial eller sekret.
Förutom av A. israelii orsakas aktinomykos också av A. naeslundi, A. viscosus, A. odontolyticus, A. meyeri och Arachnia propionica. Förekomsten av aktinomyceter i normalflora försvårar diagnosen. I den polymikrobiella genesen har särskilt Aggregatibacter actinomycetemcomitans uppmärksammats.
Epidemiologi
Aktinomykos förekommer över hela världen men den verkliga incidensen är svår att uppskatta.
