Gram Positive Bacteria Flashcards

1
Q

where are Staphylococcus found in humans?

A

Found all over the skin

Form part of the human microbiota – normal flora

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2
Q

how is staphylococcus transmitted?

A

Transmitted by direct contact, via fomites and medical instruments

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3
Q

OPPORTUNISTIC pathogens

A

Cause minor to life threatening diseases

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4
Q

Staphylococcus genus

A

Genus is:
Gram positive
Facultatively anaerobic prokaryote

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5
Q

Staphylococcus shape

A

Spherical cells-clustered like grapes- due to cell division occuring in successively different planes and daughter cells remain attached
Staphle - greek for bunch of grapes
Kokkos - berry

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6
Q

Staphylococcus tolerance

A

Salt tolerant – sweat
Tolerant to desiccation, radiation and 60 deg C-survival on environmental surfaces
Desiccation - the removal of moisture from something
Survive in dust
Produce catalase
Can different between straph and streph. As one produces catalase to neutralise

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7
Q

2 staphylococcus species commonly associated with disease in humans

A

Staphylococcus aureus -more virulent
Staphylococcus epidermidis (collective term for many species) -part of normal flora of human skin-opportunistic pathogen
Common ‘staph’ infections occur when physical barriers breached.
Physical barriers breached, by IV drip, surgery,

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8
Q

Staphylococcus aureus defences against phagocytosis x3

A

Protein A coated – binds IgG stems and inhibits complement cascade (triggered by ab mol bound to ag)

Bound coagulase on surface – forms fibrin clots – hides bacteria

Slime/capsules – polysaccharide – inhibit chemotaxis and endocytosis by leukocytes and facilitates attachment (to entry points, IV drips, catheters)

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9
Q

Staphylococcus epidermidis

A

Relies almost exclusively on slime

Opportunistic – attach to urinary catheters, intravascular catheters – form biofilms

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10
Q

enzymes produced by Staphylococcus aureus x5

A

Coagulase – fibrin threads
Hyaluronidase – breaks down hyaluronic acid – major matrix component of cells
Staphylokinase – dissolves fibrin threads
Lipases – digest lipids- allows growth on skin and in cutaneous oil glands
β lactamase – 90%

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11
Q

Staphylococcus toxins

A

Cytolytic toxins – coded by genes and disrupt cytoplasmic membranes of cells including leukocytes.

Exfoliative toxin – dissolve intercellular bridge proteins causing skin sloughing

Enterotoxins – cause vomiting associated with Staphylococcal food poisoning

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12
Q

disease caused by staphylococcus toxins

A

Toxic shock syndrome toxin - fever, rash, low bp and loss of skin (tampons)

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13
Q

Noninvasive Staphylococcus aureus infection

A

food poisoning

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14
Q

Cutaneous Staphylococcus aureus infection

A

localised pyogenic lesions, e.g. SSS, impetigo

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15
Q

Folliculitis Staphylococcus aureus infection

A

hair follicle infection with progressive stages
furuncle or boil - extension of hf to surrounding tissue
carbuncle – coalesce of furuncle – deep tissue infection – fever/chills(2nd line)

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16
Q

Bacteremia caused by Staphylococcus aureus infections

A

systemic blood infection, septic

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17
Q

Endocarditis caused by Staphylococcus aureus infections

A

life-threatening inflammation of the inner lining of your heart’s chambers and valves(endocardium).
Resulting after bacteremia circulating through heart

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18
Q

other systemic diseases caused by Staphylococcus aureus infections

A

Pneumonia and empyema

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19
Q

Osteomyelitis caused by Staphylococcus aureus infections

A

infection of bone after bad bone breakage, breaks the skin

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20
Q

Other important groups of gram positive bacteria x7

A
Streptococci – lead to scarlet fever 
Bacillus - aerobic spore producers
Clostridium
Listeria
Corynebacteria
Mycobacteria
Propionibacteria
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21
Q

Streptococci morphology

A

cocci
0.5-1.2um in diameter
Found in pairs and chains

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22
Q

characterics of streptococci

A

Gram positive cocci
Catalase negative
Facultatively anaerobic

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23
Q

Differentiation between gram positive cocci

A

Serology – reactions of antibodies to specific bacterial antigens
Haemolysis
Cell arrangement
Physiological – biochemical tests

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24
Q

Haemolysis differentiation

A

Alpha – Strep.pneumoniae & viridans streptococci

Beta – mainly Lancefield groups – Strep.pyogenes, Strep.agalactiae

Gamma – non haemolytic - Enterococci

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25
Lancefield grouping
``` Serological classification scheme Based on the bacteria’s antigens Developed 1938 – Rebecca Lancefield Groups – A to H & K to V More significant human pathogens are in Lancefield groups A, B, C, D, F & G ```
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Group A Streptococcus
AKA – GAS & S.pyogenes 1-2mm white colonies Large zone of beta haemolysis on Blood agar at 24hrs Bacitracin sensitive Pathogenic species often capsulated
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Pathogenesis of Group A Streptococcus
Evasion of phagocytosis
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Protein M
membrane protein – destabilises complement interfering with opsonisation & lysis
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Hyaluronic acid capsule
camouflage – ignored by WBCs
30
streptolysins
membrane bound proteins lyse RBCs, WBCs & platelets Interfere with oxygen-carrying capacity of blood, immunity & blood clotting After being phagocytized – release streptolysins into phagocyte cytoplasm – causes lysosomes to be released = lyses of phagocyte & release of bacteria
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Streptokinases
break down blood clots-facilitates rapid spread through infected & damaged tissue
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4 distinct deoxyribonucleases
depolymerise DNA released from dead cells in abscesses – reduces firmness of pus & facilitates spread
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C5a peptidase
breaks down C5a complement protein – acts as chemotactic factor – decreases movement of WBCs into infection site
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Hyaluronidase
breaks down hyaluronic acid- facilitating spread through tissues
35
Toxins of Group A Streptococcus
Secretion of 3 distinct pyrogenic toxins-stimulate macrophage and T helper lymphocytes to release cytokines – stimulate fever, rash & shock – aka erythrogenic toxins Toxin genes – carried on temperate phages = only lysogenised bacteria secrete
36
Epidemiology of Group A Streptococcus
Frequently infect pharynx or skin – resulting abscesses temporary – last only until specific immune responses occur against M proteins & streptolysins GAS cause disease when competing microbiota depleted – large numbers gain rapid foothold before antibodies formed or patient immunocompromised Following colonisation can invade deeper tissues & organs through barrier breaks Spread is via respiratory droplets – especially in crowded conditions Significance as pathogen declined since advent of antibiotics
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GAS diseases x7
``` Pharyngitis Scarlet fever Pyoderma & Erysypelas Streptococcal Toxic Shock Syndrome Necrotizing fasciitis Rheumatic fever Glomerulonephritis - kidneys ```
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GAS disease diagnosis
In the laboratory – Gram +ve cocci in pairs or short chains in cutaneous specimens BA or BANA – haemolytic – Lancefield group A ASOT - Anti-streptolysin O (ASO or ASLO) is the antibody made against streptolysin O, an immunogenic, oxygen-labile streptococcal hemolytic exotoxin produced by most strains of group A
39
Treatment for GAS
Penicillin Erythromycin or Cephalexin for Penicillin allergic patients Aggressive removal of non viable tissue in NF Underlying infection arrested only in immune response resulting in RF & GN Antibodies against M proteins confers long term protection but changes with strain
40
Group B streptococcus
``` S.agalactiae Bacitracin resistant Produces capsules – but targeted by antibodies – does not confer protection Predilection for newborns Produce proteases & haemolysins ```
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Epidemiology of GBS
Normally colonise lower GI tract, genital & urinary tract Maternal antibodies normally protects newborn <1 week old – early onset infection .1 week to 3 months –late onset infection Mortality can >50%
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Disease presentation of GBS
Mostly associated with > Neonatal bacteremia, meningitis & pneumonia Occurs 3/1000 newborns Mortality reduced to 5% -rapid diagnosis & supportive care 25% permanent neurological damage – blindness, deafness or mental retardation
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Diagnosis
Similar to GAS + B/C
44
treatment
Penicillin drug of choice + Streptomycin as some GBS can tolerate Pen x10 concentration CDC recommend prophylaxis to newborns whose mums colonised with GBS Immunisation
45
other Beta Haemolytic Streptococci x2
Group C – S.equisimilis (horses) – pharyngitis Group F/G – S.anginosus – purulent abscesses Penicillin effective against both
46
Viridans streptococci
Lack group specific carbohydrates | Normally inhabit mouth, pharynx, GI tract and urinary tract of humans
47
Viridans streptococci disease
Opportunistic – cause purulent abdominal infections & dental caries (dextran) – biofilm = dental plaque Once in blood can cause meningitis & endocarditis
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Streptococcus pneumoniae
Discovered 120 years ago – Louis Pasteur | Gram positive diplococcus
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Disease caused
92% of pneumococci infect humans
50
classification
Alpha haemolytic | Dimpled colony due to death of older cells
51
Treatment
Sensitive to optochin
52
Pathogenicity
Normal flora of pharynx Colonise – lungs, sinuses & middle ear Virulence = polysaccharide capsule Unencapsulated strains = avirulent 90 serotypes based on capsular antigen Produce phosphorylecholine – stimulates cells receptors (lungs/meninges/blood vessels) to engulf & hide them Could make its way to the brain, cause meningitis.
53
body defence against
Body limits migration into lungs – produces IgA – binds to organism – binds to mucous – swept away by ciliated epithelium
54
pathogens counteract
produce secretory IgA protease and pneumolysin binds to cholesterol in cytoplasmic membrane of ciliated epithelial cells & lysis cell
55
Epidemiology
Normal flora of pharynx in 75% Cause lung infections Typically highest in young & elderly – immune responses not fully active annual vaccine is available
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diseases caused
``` Pneumonia Sinusitis Otitis media Bacteremia Endocarditis Meningitis (mortality in children x20 other microorganisms) ```
57
treatment
Penicillin 1/3 now resistant – Cephalosporin, Erythromycin & Chloramphenicol Vaccine – capsular material from 23 most common pneumococcal strains Immunogenic – long lasting – except young, old & Aids patients
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other gram positive bacteria
``` Enterococci Bacillus sp Listeria Corynebacteria Mycobacteria ```
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Enterobacteriaceae
Gram negative Enteric bacteria- members of intestinal microbiota of humans and animals Ubiquitous in water, soil and decaying vegetation Some are always pathogenic while others are opportunistic pathogens Account for most nosocomial infections
60
morphology
Coccobacilli or bacilli – 1μm x 1.2-3μm
61
physiology
If motile – peritrichous flagella Some have prominent capsule, others loose slime All reduce nitrate to nitrite Ferment glucose anaerobically – although grow better aerobically All oxidase negative
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differentiation
All have similar staining properties and microscopic appearance Traditionally distinguished – biochemical tests, motility and colonial characteristics e.g MacConkey agar & Blood agar
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Pathogenicity
Outer membrane lipopolysaccharide – 3 main antigenic components a) core polysaccharide shared by all enteric bacteria-common antigen b) O polysaccharide- various antigenic varieties among strains and species e.g. Salmonella sp c) Lipid A
64
Virulence factors x7
``` Lipid A Capsules Fimbriae Exotoxins Iron binding compounds Haemolysins Type III secretion system ```
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Opportunistic coliforms
``` E.coli Klebsiella sp Serratia sp Enterobacter sp Hafnai sp Citrobacter sp ```
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Opportunistic noncoliform
Proteus sp Morganella sp Providencia sp Edwardsiella sp
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Truly pathogenic Enterobacteriaceae
Salmonella sp Shigella sp Yersinia sp
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Escherichia coli taxonomy
Domain- Bacteria Phylum- Proteobacteria Class- Gammaproteobacteria Order- Enterobacteriales Family- Enterobacteriaceae
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E.coli
Most common & important coliform Has numerous O, H & K antigens used to identify particular strains Some antigens e.g. O157 associated with virulence Virulence plasmids – can be transferred
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virulent e.coli
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diseases caused by e.coli
UTI’s Neonatal meningitis Gastroenteritis- exotoxin called enterotoxin – bind proteins on intestinal tract cell lining – portion enters cell and triggers a series of chemical reactions - results in loss of electrolytes producing watery d & v – a common cause of paediatric infections on developing countries. Severe to fatal hemorrhagic colitis
72
Vero toxin (VT), or Vero cytotoxin
The E coli strains associated with hemorrhagic colitis (enterohemorrhagic E coli, or EHEC) most notably O157:H7, produce relatively large amounts of the bacteriophage-mediated Shiga-like toxin. This toxin is called Vero toxin (VT), or Vero cytotoxin after its cytotoxic effect on cultured Vero cells. Many strains of O157:H7 also produce a second cytotoxin (Shiga-like toxin 2, or Vero toxin 2), which is similar in effect but antigenically different.
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Truly Pathogenic Enterobacteriaceae X3
Not considered members of normal microbiota of humans – almost always pathogenic due to their virulence factors All 3 synthesize type III secretion systems > Salmonella > Shigella > Yesinia
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salmonella
Gram-negative facultatively anaerobic predominantly motile by peritrichous flagella over 2200 strains identified all species are pathogenic to both humans and other animals complex cycle of transmission
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main reservoir of salmonella bacteria
intestinal tract of birds and animals sewage, fertilisers and slurry animal feeds human carriers
76
foods that could be contaminated
``` meat and meat products milk and milk products eggs and egg products fish confectionery miscellaneous foods - dried yeast, frogs legs, marijuana, peanut butter ```
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clinical features of Enteritis
diarrhoea, abdominal pain, mild fever, chills, nausea, vomiting incubation period of 5-72 hours, but occasionally up to 7 days lasts 2-5 days infective dose varies from as little as 50 cells to 1,000,000 per gram of food
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Enteric Fevers
some species can cause more serious infections eg. S. typhi and S. paratyphi.
79
Pathogenicity
Salmonellae adhere to the epithelial lining of the ileum by means of fimbriae followed by invasion and multiplication Toxin production: endotoxin, 3 enterotoxins, cytotoxin
80
prevention
joint action by agriculture and food sectors of industry and also by the consumer control starts on the farm and continues through the food chain to the consumer
81
S.typhi infection through body
Humans sole hosts Infection via ingestion of contaminated food or water Bacteria pass through intestinal wall to bloodstream Phagoscytised but not killed and carried to liver, spleen, bone marrow & gallbladder Bacteria released from gallbladder to re-infect the intestines – resulting in gastroenteritis abdominal pain & recurring bacteremia In some bacteria ulcerate and perforate intestinal wall causing peritonitis in abdominal cavity.
82
S.typhi symptoms
Patients have increasing symptoms of fever, headache, malaise, muscle pain & loss of appetite – lasts about a week
83
Shigella
Genus of Gram-negative, non-spore forming rod-shaped bacteria closely related to Escherichia coli and Salmonella. The causative agent of human shigellosis Shigella cause disease in primates, but not in other mammals
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Classification
Serogroup A: S. dysenteriae (12 serotypes) Serogroup B: S. flexneri (6 serotypes) Serogroup C: S. boydii(23 serotypes) Serogroup D: S. sonnei (1 serotype)
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S. flexneri
is the most frequently isolated species worldwide | accounts for 60% of cases in the developing world;
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S. sonnei
causes 77% of cases in the developed world, compared to only 15% of cases in the developing world;
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S. dysenteriae
is usually the cause of epidemics of dysentery, particularly in confined populations such as refugee camps.
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shigella infection
Shigella infection is typically via ingestion (fecal–oral contamination); depending on age and condition of the host as few as ten bacterial cells can be enough to cause an infection.
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disease presentation of shigella infection
Shigella causes dysentery that results in the destruction of the epithelial cells of the intestinal mucosa in the cecum and rectum.
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Shiga toxin
Some strains produce enterotoxin & Shiga toxin, similar to the verotoxin of E. coli O157:H7. Both Shiga toxin and verotoxin are associated with causing hemolytic uremic syndrome.
91
treatment
Replacing fluids & electrolytes Oral antibiotics can be given to reduce the spread in close contacts – e.g.Ciprofloxacin & cephalosprins Vaccine (live attenuated) being developed with some success against S. flexneri
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Yersinia genus
Genus contains 3 notable species Y. enterocolitica Y. pseudotuberculosis Y. pestis
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pathogenesis
Normally pathogens of animals All 3 contain virulence plasmids that code for adhesins & type III systems Y. enterocolitica & Y. pseudotuberculosis (less severeform) are enteric pathogens acquired via consumption of contaminated food or water by animal faeces. Y. enterocolitica occurs most often in young children.
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symptoms
Common symptoms in children are fever, abdominal pain, and diarrhea, which is often bloody. Symptoms typically develop 4 to 7 days after exposure and may last 1 to 3 weeks or longer. In older children and adults, right-sided abdominal pain and fever may be the predominant symptoms, and may be confused with appendicitis due to inflammation of mesenteric lymph nodes
95
Yersinia pestis
Plague is an infectious disease of animals and humans caused by a bacterium named Yersinia pestis. People usually get plague from being bitten by a rodent flea that is carrying the plague bacterium or by handling an infected animal. fully treatable with antibiotics
96
Bubonic plague
painful swollen lymph nodes – bacteremia results in DIC, subcutaneous hemorrhaging & tissue death – ‘Black Death’
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Pneumonic plague
pulmonary distress within a day – can spread person to person via aerosols & sputum
98
other gram negative bacteria
``` The Pasteurellaceae (oxidase pos) Haemophilus sp – require growth factors Bartonella Brucella Bordetella Burkholderia Pseudomonads ```
99
toxic forms of oxygen
highly reactive because in the same way that oxygen is the final oxygen acceptor for aerobes, they are excellent oxidizing agents, i.e. they steal electrons from other compounds
100
how oxygen cause damage
electron depleted compounds then steal electrons from other compounds Resulting in a chain of vigorous oxidation Causing irreparable damage to cells by oxidizing important compounds including proteins and lipids
101
Singlet oxygen (1O2)
Molecular oxygen – electrons boosted to a higher energy state – during aerobic metabolism A very reactive oxidizing agent Phagocytic cells – certain human white blood cells use it to oxidize pathogens
102
Superoxide radical (O2-)
Superoxide radicals form during incomplete reduction of O2 during electron transport in aerobes and during metabolism by anaerobes in the presence of oxygen Aerobic organisms produce superoxide dismutase to detoxify them – lacking in anaerobes Have active sites that contain metal ions e.g. Zn2+ and Fe2+ Combine 2 superoxide radicals and 2 protons to form hydrogen peroxide (H2O2) and oxygen
103
Peroxide anion (O22-)
Hydrogen peroxide produced during reactions catalysed by superoxide dismutase Peroxide anion makes hydrogen peroxide an antimicrobial agent Aerobes have either catalase or peroxidase to detoxify the peroxidase anion
104
Hydroxyl radical (OH)
Hydroxyl radicals result from ionizing radiation and from incomplete reduction of hydrogen peroxide Most reactive of the 4 Due to catalase and peroxidase effect eliminated in aerobes
105
Facultative anaerobes
Can live in various oxygen concentrations Can maintain life via fermentation or anaerobic respiration Metabolic efficiency reduced in absence of oxygen e.g. E.coli
106
Aerotolerant anaerobes
Do not use aerobic metabolism Have some detoxifying enzymes e.g. lactobacilli
107
Microaerophiles
Microaerophiles are damaged by the 21% concentration of atmospheric oxygen Some organisms require oxygen levels of 2% to 10% e.g. Helicobacter pylori – ulcer causing pathogen – concentration of oxygen in stomach 2-10%
108
Injecting Drug User (IDU) Infections
40% of IDU hospital admissions due to infections, 20% result in death Intravenous, intra-muscular or subcutaneous injection Minor bacterial infections usually result in local abscess formation Severe illness if the injected material or paraphernalia, are contaminated with certain clostridial spores
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Clostridia
Gram positive anaerobic spore-forming rods
110
pathogenic clostridia
``` C. perfringens C. septicum C. sordellii C. novyi C. histolyticum C. tetani C. botulinum C. difficile ```
111
distribution of clostridia
Widely distributed in soil and gut Resistant to environmental conditions Exist as exo-spores Spores germinate when introduced into an oxygen-reduced environment Pathogenic species may release powerful exotoxins
112
contamination of clostridia
Injuries as a result of warfare Shrapnel wounds Soil and faeces are the prime sources of clostridial spores Practice of injecting substances into muscle tissue mimics the risk of infection associated with the trauma of warfare
113
IDU Outbreak, 2000
Cases of serious illness and deaths amongst IDUs recorded in parts of UK 60 IDUs in Scotland acquired a severe infection at or near an injection site Spread rapidly Extensive skin and muscle damage Hypotension Multi-organ failure 23 deaths Association with a batch of heroin in circulation at the time and the practice of skin or muscle “popping”
114
clinical presentation of drug related infection
Soft tissue inflammation at injection site > Abscess, Cellulitis, Fasciitis, Myositis Local inflammatory reaction has varied > Minimal pain and swelling at injection site Severe local symptoms > Extensive swelling, Pain, Oedema, Erythema with blackening/blistering at centre, Extensive necrosis, Necrotising fasciitis
115
infection of heroin injection
Veins become damaged after long periods of use, other areas of body may be used for injecting > Groin area > Behind the knees > Neck Bacterial contaminants of the injectate that survive can cause infections in users who inject by skin or muscle popping Bacterial spores were suspected to be of potential importance in infections
116
C.novyi Type A
Widely distributed in soil Examine anaerobic cultures after 24h incubation for small, flat, rough or rhizoidal, translucent, haemolytic colonies with a spreading edge Exposure to air toxic to micro-colonies that haven’t begun sporulation After 48-72h, colonies often coalesce to give a fine spreading growth  Gram-variable rods, some with sub-terminal spores Unreactive in commercial anaerobe identification kits (API Anaerobe)
117
C.perfringens
Post-mortem contaminant Large discrete colonies after 24h incubation Flat and rough-edged, or smooth and domed Non-haemolytic or with a narrow zone of complete haemolysis inside a larger zone of partial haemolysis Straight-sided, gram variable rods, no spores
118
C.septicum
Grows rapidly Thick, swarming growth, haemolytic Gram variable rods, numerous sub-terminal spores Most common source of isolates from blood cultures of patients with malignancies of the colon
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C.botulinum
Proteolytic types A,B and F initially produce discrete rhizoidal colonies that spread and coalesce Haemolysis is variable Profuse sub-terminal and free spores, gram variable bacilli Implicated in food-borne illnesses and cases of wound botulism
120
C.tetani
Uncommon in recent decades Outbreak between July ‘03 and March ‘04, 22 cases in IDUs Colonies may produce a fine swarming growth Gram stain of overnight cultures can give readily over-decolorised long bacilli without spores Classical ‘drumstick’ appearance of cells with terminal, round spores after further incubation
121
Treatment
Early surgical intervention > Exploration, Drainage, Extensive debridement Microbiological sampling Patients presenting with compartment syndrome > Urgent decompression > Excision of surrounding oedematous tissues Antimicrobial therapy > Penicillin, Metronidazole, Clindamycin