Microbiology Flashcards
RNA viruses
Hep A, C, D, E
Rubella
Zika
(all single stranded)
Rotavirus is double stranded
HIV is a retrovirus
DNA viruses
VZV
HSV
Hep B
CMV
HPV
EBV
(all double stranded)
Parvovirus is single stranded
Bacteria
Prokaryotic (no membrane-bound organelles)
Visible by light microsopy, average diameter 1μm
Cell wall made of N-acetyl glucosamine/muramic acid, peptidoglycans (penicillin binding sites, target for β-lactams), polypeptides and polysaccharides
BACTERIAL GROUPS
Gram stainable - +ve or -ve or variable
Acid-fast bacilli - cell wall has high lipid content so difficult to stain (mycobacteria, norcardia)
Unusual - no peptidoglycans (chlamydia, mycoplasma)
Taxonomy of bacteria
By shape - bacilli (rods) or cocci (grains)
By O2 requirement - aerobes or anaerobes (anaerobes can be facultative so capable of aerobic respiration if O2 is present, OR obligate anaerobes which die in presence of O2
By spore forming
By staining
Gram staining
Stain with crystal violet, then Gram’s iodine, decolourize with acetone, then counter-stain with methyl red
Gram +ve stain blue, retaining crystal violet stain
- due to peptidoglycan, a thick polysaccharide coat that loses stain very slowly once taken up
Gram -ve stain pink, as cell wall is thinner so doesn’t retain crystal violet but does take up methyl red stain
- cell wall consists of outer layer of LPS, then periplasmic layer containing β-lactamase, then inner peptidoglycan layer
Gram +ve bacteria examples
Cocci
- staphylococcus (form grape-like clusters)
- streptococcus (form chains)
Bacilli
- clostridium
- listeria
- bacillus
Gram -ve bacteria examples
Cocci
- neisseria gonorhoeae
- neisseria meningitidis
- moraxella catarrhalis
Bacilli
- haemophilus influenzae
- klebsiella pneumoniae
- legionella
- escherichia coli
Spirochaetes
- leptospira
- borellia (lyme)
- treponema (syphilis)
Vibrio
- cholera
Can also be divided based on lactose fermentation (klebsiella, Ecoli, enterobacter) which stain orange on McConkey agar
Bacterial toxins
Exotoxins
- secreted by organisms
- highly antigenic, destroyed by heat
- gram +ve (or -ve) produce
- form toxoids
Endotoxins
- released on cell death and lysis
- grame -ve only eg E coli
- mainly lipid A from LPS
Bacterial antimicrobial resistance
Bacterial mechanisms
- drug inactivation (eg production of β-lactamase
- alteration of drug target site (eg alteration on penicillin-binding sites)
- bacterium metabolic pathway alteration
- fibronectin coat
- IgA cleaving protease
Mechanisms of transfer of resistance - horizontal (plasma DNA transfer, chromosomal mediated resistance, bacterial conjugation) or vertical
Vaginal flora
Influenced by oestrogen levels
-> increased vaginal glycogen concentration
- pH 3.5-4.5 due to conversion of glycogen to lactic acid by lactobacilli
Clinical isolation of bacteria
Use of specific microbiological swabs
Storage at 4degrees
Preliminary lab report takes 18hours
Identification via detection of antigens, antibodies, nucleic acids
Streptococcus
Gram +ve
Mostly facultative anaerobes (can survive in either)
Catalase negative or oxidase negative
Form chains
Produce exotoxins
3 groups based on levels of haemolysis when cultured on horse blood agar:
- non-haemolytic - E.faecalis
- partial haemolytic - S.viridans, enterococcus, pneumococcus
- complete haemolytic (β)- group A/C/G, group B, group F
β-haemolytic streptococci
Gram +ve
Subdivided by Lancefield grouping A-O
Group A, C, G - associated with toxic shock syndrome, necrotizing fasciitis, vaginitis
Group B - chorioamnionitis, neonatal sepsis, endometritis
Group F - can cause abscesses
Group A streptococcus
= strep pyogenes
(type of β-haemolytic gram +ve)
Virulence factor determined by presence of M protein (fimbrial protein involved in capsule formation, anti-phagocytic, responsible for organism adhesion and invasion), hyaluronidase, streptokinase, DNAse, superantigens
Causes - scarlet fever, toxic shock, rheumatic fever, glomerulonephritis, necrotizing fasciitis
Group B streptococcus
= streptococcus agalactia
(type of β-haemolytic gram +ve)
20-35% women carry, intermittent
Maternal to fetal transmission 80%, with invasive neonatal disease 0.5/1000 births
6% neonatal mortality rate from early-onset GBS disease in UK
Indications for antibiotic prophylaxis during labour
- early-onset GBS disease in previous baby
- GBS in vagina/urine during pregnancy
- prolonged ROM at term (>18hr)
- preterm labour <37weeks
- preterm ROM with known GBS
- intrapartum pyrexia
-> Benpen 3g IV loading dose then 1.5g IV 4hrly until delivery
(or clinda 900mg IV 8hrly, or erythromycin 500mg 6hrly, vancomycin last resort)
Streptococcus pneumoniae
Partial haemolytic gram +ve
Diplococcus - forms pairs
Draughtsman-shaped colonies
Optochin sensitive
Bile soluble
-> meningitis, pneumonia, primary bacterial peritonitis (pre-pubertal girls)
Enterococcus
Partial haemolytic gram +ve
E.faecalis or E.faecium
GI commensal organisms
Resistant to many antimicrobials
-> endocarditis, proctitis
Listeria monocytogenes
Gram +ve bacilli
1/10,000 pregnant women
Some strains β-haemolytic
Produces flagella at room temperature, but not 37degrees
Listeriosis -> meningitis, hepatosplenomegaly, bradycardia
Transmitted in contaminated food
To the fetus via transplacental spread or ascending infection
In placenta -> miliary granuloma, focal necrosis
50% fetal mortality rate
Treatment - amoxicillin or gentamicin, 3 weeks
Staphylococcus
Gram +ve cocci
Facultative anaerobes
Form grape-like clusters
Classified on ability to form coagulase
-> scalded skin syndrome, toxic shock, slime in IV cannula
eg MRSA is coag +ve, DNAse +ve, catalase +ve
Actinomycetes israelii
Gram +ve anaerobe bacillus
Shows branching
Slow growing
In mouth, IUCDs
-> chronic granulomatous disease by produces sulphur granules in tissues
Treat with penicillin, 6-12mo therapy
Neisseria
Gram -ve diplococci
-> meningitis, gonorrhoea
Capnophilic (thrive in presence of high CO2)
Treat with cephalexin
Multidrug resistance is growing
Gonorrhoea
Neisseria gonorrhoeae (gram -ve intracellular diplococci)
Infects mucus membranes of urethra, endocervix, rectum, pharynx, conjunctiva (can also Bartholin’s)
Complications - gonococcal ophthalmia neonatorum (conjunctivitis), neonatal vaginitis/proctitis/urethritis, disseminated gonococcal infection
Treatment - IM ceftriaxone 250mg stat OR PO cefixime 400mg
Needs test of cure 3 days after treatment
40% also have concurrent chlamydia
Gardnerella vaginalis
Facultative anaerobe
Gram variable
Bacillus
Normal commensal organism of vagina
β-haemolytic
Bacterial vaginosis
Polymicrobial condition characterized by:
- depletion of protective lactobacillus species
- increase in other organisms esp anaerobes, eg G.vaginalis, mobincullus, atopobium vaginale
60% asymptomatic
More common in black women
Aetiology unknown
Assoc with mid-trimester miscarriage, pre-term birth, ROM, endometritis
Treat with metronidazole 400mg BD for 7days
Amsel and Hay/Ison criteria
AMSEL
For diagnosis of BV, need 3/4:
- vaginal discharge
- clue cells
- pH>4.5
- fishy odour with alkali on wet mount
HAY/ISON based on gram stain
- Grade 1 = normal flora, mostly lactobacilli
- Grade 2 = mixed flora
- Grade 3 = BV, absent lactobacilli
Typically fishy white/grey vaginal discharge worse after intercourse
Syphilis microbiology and treatment
Gram -ve spirochaete Treponema pallidum
Cannot be cultured in lab
Serology indistinguishable from yaw and pinta
Treatment - penicillin G, doxycycline
- watch for Jarisch-Herxheimer reaction (due to release of cytokines when antibiotics kills bacteria)
Syphilis stages
PRIMARY
- chancre (painLESS ulcer)
- appears 10-90days post exposure, persists 4-6weeks before disappearing
SECONDARY
- 1-6months after primary infection
- symmetrical non-itchy rash on trunk, condylomata latum (white/grey lesions), mucous patches around genitals or mouth
TERTIARY
- 1-10years after initial infection
- gummas (soft rubbery growth, granuloma with necrotic centre), neurosyphilis, de Musset’s sign (head nod in time with heart beat)
Can -> endarteritis obliterans
Test for syphilis
Hard to distinguish between active, and treated past infection
Non-specific tests - Veneral disease research laboratory (VDRL), rapid plasma reagin, Wasserman’s reaction, Hinton’s test
Specific tests - fluorescent treponemal antibody-absorption test (FTA-ABS), and treponema pallidum agglutination assay (TPPA)
False +ve with non-specific tests in viral infections, lymphoma, TB, malaria, pregnancy
Mycoplasma hominis
In 20% of sexually active women
Can either be a primary or co-pathogen in PID
Can cause postpartum pyrexia
Can be co-pathogen in chorioamnionitis
Treat - doxycycline / clindamycin
Chlamydia trachomatis
Obligate intracellular grame -ve organism
3 subgroups:
- A-C (follicular conjunctivitis)
- D-K (genital)
- L1-L3 (lymphogranuloma venereum)
Contains DNA and RNA
72hr lifecycle, elementary body -> reticular body -> inclusion body
Treatment - doxycycline / azithromycin / erythromycin / ofloxacin
Test of cure only in pregnant or breastfeeding women
Vaginal discharge in children causes
Foreign body (commonest)
Strep pyogenes
Haem influenza
Shigella sonei
Pinworms
Chlamydia
N gonorrhoeae
Wound infection
Usually staph aureus - give fluclox
Typically require 10^5 organisms to establish
If foreign body present, only need 10^3
Necrotizing fasciitis
Type 1
- assoc with surgery, diabetes
- due to polymicrobial infection, anaerobes facultative or obligate
Type 2
- due to group A strep
Treatment
- surgical debridement
- antibiotic combination of Benpen 1.2g IV QDS, clindamycin, ciprofloxacin
- surgical re-exploration of wound
Pelvic inflammatory disease symptoms and complications
Pelvic / abdominal pain
Dyspareunia
Post-coital bleeding
Discharge
Cervical tenderness
Fever
Complications
- ectopic pregnancy
- tubal infertility (12% 1st episode, 20% 2nd, 50% 3rd)
- chronic pelvic pain
- Fitz-Hugh-Curtis syndrome (adhesions causing RUQ pain and perihepatitis)
Causative organisms and treatment of PID
Organisms - chlamydia, neisseria (gonorrhoea), mycoplasma hominis/ureaplasma, gardnerella, trichomonas vaginalis, GBS
Treatment:
OP
- ofloxacin 400mg BD + metronidazole 400mg BD for 14 days OR
- IM ceftriazone 250mg then PO doxy 100mg BD + metro 400mg BD for 14 days
Reiter’s syndrome
Reactive arthritis caused by bacterial infection
Can’t pee, see, climb a tree:
Urethritis, uveitis, arthritis
Causative organisms - salmonella, yersinia, shigella, campylobacter, chlamydia, gonorrhoea
Fungi
Multicellular eukaryotic (membrane-bound organelles)
Aerobic
Cell walls have no peptidoglycans but contain ergosterol
Contain - fibrils, chitins, mannan, glucan
Asexual and sexual reproduction
Secrete keratinase
MOULDS - multicellular, branching filament (hyphae/mycelia), reproduce by spores, eg aspergillus
TRUE YEASTS - unicellular, reproduce by budding, eg cryptococcus
YEAST LIKE - eg candida
DIMORPHIC - grows as yeast at 37degrees, as mycelia at 20degrees, eg histoplasma
Protozoa
Unicellular, eukaryotic, free-living organisms
Include trichomonas vaginalis, toxoplasma gondii, giardia, cryptosporidium, plasmodium
Asexual or sexual reproduction
True protozoa and helminths (fluke = trematode, tape = cessatode, ring = nematode)
Trichomonas vaginalis
Flagellate protozoon
Venereal transmission (STI)
Diagnose - wet prep, PCR, culture
Symptoms - discharge, intense itching and irritation, strawberry cervix, preterm delivery
Treatment - metronidazole or tinidazole
Toxoplasma gondii
Zoonotic infection - mainly cats
Diagnosis - IgA/M avidity, serial samples taken 3weeks apart
Affects muscle, neural tissue, placenta
Transmission via placenta in primary infection, greatest risk at 26-40weeks BUT the earlier the infection occurs the more severe the disease in the newborn
Maternal risk of chorioretinitis and encephalitis
Congenital infection - stillbirth, cerebral calcification, microcephaly/hydrocephalus, choroidoretinitis, cerebral palsy, epilepsy, hepatosplenomegaly, thrombocytopenia
Toxoplasma IgM persists for 3years after eradications
Malaria
From female Anopheles mosquito vector
Infects RBCs
Plasmodium falciparum / vivax / ovale / malariae / knowlesi
Severe malaria if parasitaemia >2%
Clinical features - fever, resp distress/pulm oedema, arthralgia, retinal damage, splenomegaly, hepatomegaly, haemoglobinuria and renal failure, coma, convulsions, 20% mortality in non-pregnant but 50% in pregnant
Biochemical abnormalities -hypoglycaemia, anaemia, thrombocytopenia, acidosis, hyperlacatataemia
Fetal effects - miscarriage, stillbirth, prem, placental parasitaemia
Diagnosis and management of malaria
Diagnosis via thin and thick blood films
Management:
- vector control - insecticides, mosquito nets, skin repellents
- chemo-prophylaxis - mefloquine, doxycycline, malarone, quinine
- treatment - quinine, chloroquinine, artermisinin
Viruses
No organelles
Depend on host for energy metabolism and protein synthesis
Genetic material is either RNA or DNA
Viral coat = capsid
Fetal transmission rate increases with gestational age
Incubation period usually 21days ish
CMV
Part of herpes family
50-80% women are seropositive
Feto-maternal transmission 40%, symptomatic in 10%
Maternal infection diagnosed with IgG avidity (high = old infection)
Congenital defects - sensorineural hearing loss, retinitis, cerebral palsy, hepatosplenomegaly, hyperbilirubinaemia, intracranial calcification, thrombocytopenia, FGR, microcephaly
CMV IgM persists for months/years
Herpes simplex
Type 1 - 30% genital infections in UK
Type 2 - 70%
Fetal transmission >30% if primary infection in 3rdT
- 2% if secondary episode during labour
High fetal mortality, so relative indication for caesarean if maternal lesions present within 6 weeks of birth, as long as no ROM
21 day incubation
Affects skin, eyes, mouth, CNS
If first episode in 1st or 2nd T - treat with normal 5 day course aciclovir 400mg TDS, then give prophylactically again from 36w-delivery
If first episode in 3rdT give until delivery, and recommend caesarean
Varicella Zoster
Part of herpes family
- contagious 48hr pre rash, incubates 10-21 days
Fetal transmission (congenital fetal varicella syndrome) only in first 20weeks
- overall rate 1%, higher at 13-20weeks
- CNS anomaly (microcephaly, cortical atrophy), limb hypoplasia, cicatricial scarring, eye defects (microphthalmia, cataracts, chorioretinitis)
Risk of neonatal varicella if maternal infection within 10days of delivery
Maternal complications - pneumonitis, encephalitis, hepatitis
Treatment
- maternal infection -> aciclovir
- exposed to VZV -> prevention of disease with VZIgG
Rubella
RNA virus
aka German measles
Togavirus
Single-stranded RNA genome enclosed in capsid
Spreads via droplets
Congenital - eye (cataracts, glaucoma), heart (PDA, VSD, pulm stenosis), sensorineural hearing loss, haematological (thrombocytopenic purpura, haem anaemia, lymphadenopathy), ‘blueberry muffin’ rash
Feto-maternal transmission rate 90% in 1stT, 30% in 2ndT
In 1stT, 90% of those infected develop defects. >20 weeks no increased risk to fetus.
Parvovirus B19
Single stranded DNA virus
aka fifth disease / slapped cheek syndrome / erythema infectiosum
Incubation 4-14 days
60% women are immune
Causes miscarriage (10%), hydrops fetalis
NO congenital defects
Fetal transmission 30% in 1stT
Treat with intrauterine fetal blood transfusion
Virus attacks P blood group antigen (globiside) on RBCs and fetal heart
HIV
Lentivirus (RNA retrovirus)
Primarily infects Th cells (CD4 esp), macrophages, dendritic cells, via gp120 glycoprotein
AIDS is when CD4 count <200. Complications include Kaposi’s sarcoma, pneumocystis carinii pneumonia, Non-Hodgkin’s lymphoma, dementia
Transmission is sexual, blood products, perinatal
+ possibly from saliva, tears or urine - negligible risk
0.17% of UK antenatal population are +ve
Fetal transmission rate is 15% without treatment, <1% with
- increased vertical transmission if high maternal viral load, low CD4 count, PROM, chorioamnionitis, co-morbid viral infection, breastfeeding, pre-term
- ALL mothers advised not to breastfeed
- increased risk miscarriage, preterm, IUGR
HIV structure
120nm diameter
2 copies of single-stranded RNA enclosed by capsid
Capsid is viral protein p24 and matrix of viral protein p17
Viral envelope surrounds the matrix, composed of phospholipids and glycoprotein
Glycoprotein enables virus to attach to and fuse with target cells
HPV
5 groups: α / β / γ / Nu / Mu-papillomaviruses
α-papillomaviruses have 2 subtypes:
- low-risk 6 and 11 -> non-malignant change
- high-risk 16, 18, 31, 33, 45 (via E6 and E7 oncogenes) -> malignant change
Only infect epithelial cells
Structure is 75 capsomeres, each consist of 5 molecules of L1 co-protein, containing circular DNA (double stranded)
- genome of early and late proteins
- causes inactivation of p53 and pRB
- incubation period 2-8months
- regresses spontaneously via cell-mediated immunity (70% within 1 year)
- treatment - podophyllotoxin, imiquimod, cryotherapy
Hepatitis viruses
Hep A - maternal-fetal transmission rare
Hep B - incubation 6w-6mo
- antigen detection with time progresses surface -> core -> eAntigen
- antibody production (IgM) core -> eAntigen -> surface
- immunity confirmed with anti-surface IgM
- vertical transmission via pregnancy, labour and lactation. Rates depend on viral load and antigen profile
- if e-antigen +ve then 90% transmission, if surface-antigen +ve then 20%
- mostly in 3rdT
- can treat with Interferon α or Lamivudine
- give neonate propyhlactic hepB vaccine and IgG
Hep C - increased risk obstetric cholestasis, 3-5% vertical transmission
Hep E - 5% maternal mortality, fulminant hepatic failure in pregnancy 20%
Hepatitis B serology
HBsAg (surface antigen)
+ve in acute and chronic infection, -ve if immune or post vaccination
HBeAG (e antigen)
+ve in acute early infection, -ve in chronic/immune/post vaccination
IgM anti-core antibody
+ve in acute infection, -ve in chronic /immun/post vaccination
IgG anti-core antibody
+ve in acute, chronic and immune, negative post vaccination
HepB virus DNA
+ve in acute early and chronic (high infectivity) but -ve in acute resolving, chronic (low infectivity), immune or post vaccination
Anti-HBe Ab
-ve in acute early and post vaccination, can be +ve or -ve otherwise
Anti-HBs Ab
-ve in acute and chronic infection, +ve post vaccination
HTLV
= human T-lymphotropic virus
0.25% in UK
Feto-maternal transmission via breast milk
Manifestations of congenital infections occur after 10-30 years with T-cell leukaemia, or tropical spastic paraparesis
Antibiotic mode of action
Penicillins
- Beta-Lactam inhibit peptidoglycan cross-links in bacterial cell wall
- Amoxicillin, Phenoxymethylpenicillin, Flucloxacillin
Cephalosporins
- Beta-Lactam inhibit peptidoglycan cross-links in bacterial cell wall
- Cefalexin,
Ceftriaxone,
Cefuroxime
Macrolides
- Peptidyltransferase Inhibitor
- Erythromycin, Clarithromycin, Azithromycin
Quinolones
- DNA Gyrase Inhibitor
- Ciprofloxacin, Levofloxacin, Moxifloxacin
Tetracyclines
- Bind to 30S subunit of microbial ribosomes blocking attachment of aminoacyl-tRNA to the A site on the ribosome
- Lymecycline, Oxytetracyline, Doxycycline
Nitrofurantoin
- Damages bacterial DNA via multiple reactive intermediaries
Trimethoprim
- Dihydrofolate Reductase Inhibitor
Molloscum contagiosum
- viral infection of the skin and occasionally mucous membranes
- most on trunk, arms, groin, and legs
- DNA poxvirus MCV, has no non human reservoir
- spread from person to person by touching the affected skin
- RFs - sexually active, immunodeficient
- contagious until the bumps are gone. Some growths may remain for up to 4 years if not treated
- lesions are flesh-colored, dome-shaped, and pearly in appearance, 1–5 mm in diameter, with a dimpled center, generally not painful, but they may itch or become irritated
- treatment is supportive
Toxic shock syndrome
Rare, life-threatening sudden inflammatory response syndrome with fever, rash, hypotension, multi-organ involvement
- assoc with tampons
- usually Staphylococcus aureus -> exotoxin TSST-1
- also streptococcus pyogenes exotoxin A (SPEA) and S pyogenes exotoxin B (SPEB) by group A beta-hemolytic streptococci
- toxins activate production of cytokines, such as tumor necrosis factor, interleukin-1, M protein, and gamma-interferon and induction of nitric oxide production which contributes to hypotension
MRSA treatment
Best responds to vancomycin or teicoplanin
Resistant to penicillins
Controlled by chlorhexadine wash and mupirocin ointments
Beta-lactam antibiotics
eg penicillins and cephalosporins (cefalexin, ceftriaxone)
- inhibit bacterial cell wall synthesis by interfering with linking of soluble peptidoglycan precursors
- analogues of d-alanyl-d-alanine
- effective against all gram positive bacteria and gram negative cocci
- excreted by the kidneys
- resistance mainly via beta-lactamase production
Glycopeptide antibiotics
Vancomycin and teicoplanin
- inhibit bacterial cell wall synthesis by binding to d-alanyl-d-alanine at the end of a pentapeptide chain, preventing the incorporation of new subunits
- cannot penetrate gram negative cell wall, only work against gram positive bacteria
- not absorbed from the GI tract. Oral administration used to treat Clostridium difficile diarrhoea
- potentially ototoxic and nephrotoxic - vancomycin should be administered slowly to prevent ‘red-man’ syndrome. Teicoplanin is less toxic and can be given bolus
Aminoglycoside antibiotics
Gentamicin, tobramycin, netilmicin by 30s subunit
- not absorbed from the GI tract. Do not cross the blood-brain barrier
- not active against streptococci. Active against gram negative bacteria
- excreted via the kidneys
- potentially ototoxic and nephrotoxic
- production of aminoglycoside modifying enzymes is the most important mechanism of acquired bacterial resistance - usually plasmid mediated
Tetracycline antibiotics
Doxycycline
- inhibit bacterial protein synthesis by 30s subunit
- absorbed from the gut
- penetrate tissues well and are active against intracellular bacteria
- effective against chlamydial, mycoplasma and rickettsiae infections
- cross placenta - interferes with bone development and cause brown discolouration of teeth - contraindicated in pregnancy and children
- widespread resistance as a result of their use as growth promoters in animal feed - resistance gene carried on a transposon
Chloramphenicol
- inhibits bacterial protein synthesis by blocking peptidyl transferase, 50s ribosome
- well absorbed from the gut
- active against a wide range of bacteria. Main indication is the treatment of Salmonella typhi
- causes REVERSIBLE dose-dependent bone marrow suppression
Macroglide antibiotics
Erythromycin, azithromycin, clarithromycin and spiramycin
- inhibit bacterial protein synthesis by binding to 23S rRNA (on 50s)
- well absorbed from the gut; penetrate tissues well and are active against intracellular organisms
- erythromycin is concentrated in the liver and excreted via bile
Clindamycin
In group of Lincosamides
- binds to 50S ribosomal subunit
- similar antibiotic spectrum to erythromycin, excreted by the liver, active in faeces for up to 5 days after a dose
- more active against anaerobes than erythromycin. Clostridium difficile is resistant and may be selected, causing pseudomembranous colitis
Iodine
- excellent activity against gram positive and most gram negative bacteria
- excellent activity against TB, viruses
- good activity against fungi
- poorer activity against endospores and markedly affected by organic matter
- not suitable for use as surgical scrub but can be used for skin prep. Can burn skin so should be removed after several minutes
- not suitable for use on mucous membranes
- iodine may be absorbed by the neonate and affect thyroid function
Chlorhexadine
- excellent activity against gram positive bacteria but less effective against most gram negative bacteria
- excellent activity against viruses
- poor activity against TB and fungi, no activity against endospores
- only slightly affected by organic matter
- useful as surgical scrub and skin prep – has high persistent activity
- suitable for use on mucous membranes
- toxic to ears and eyes
- combination with detergents highly effective for hand disinfection.
Obligate anaerobes
Clostridium - gram positive
Bacteroides - (also called Prevotella) gram negative
