classification of pathogenic bacteria, pathogens & host Flashcards

1
Q

gram’s stain

A
  • Quick, simple, inexpensive way to classify clinically important organisms - Provides an early indication of the genus of bacteria that may be causing infection ○ Combine knowledge from gram stain with morphology - Different species have varying capacity to cause disease (pathogenicity)Different classes of antibiotics are effective against gram +ve and -ve bacteria (targeted treatment)
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2
Q

cells wall differences in gram +ve vs -ve bacteria

A

Thick peptidoglycan layer in gram +ve Thin peptidoglycan layer, more complex cell wall, thick lipopolysaccharide layer in gram -ve

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3
Q

classification of gram +ve bacteria

A

stain purple2 major types of classification are aerobic/anaerobic or their morphology (cocci/bacilli) Chains - streptococcus Clusters - staphylococci Streptococcus - how do they grow on blood agar Partial/complete/no haemolysis

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4
Q

coagulase +ve gram +ve bacteria

A

staphylococcus aureus

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5
Q

staphylococcus aureus

A

○ Commensal organism carried in nose, axilla and perineum ○ Major human pathogen causing a wide range of disease boils/abscesses and soft tissue infections to septicaemia and osteomyelitis - Commonly penicillin resistant due to production of penicillinase- By a different mechanism, some strains are methicillin resistant MRSA poses major problems for infection prevention and control in hospitals

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6
Q

coagulase -ve gram +ve bacteria

A
  • many different species (staphylococcus S. epidermis, S. haemolyticus, S. saprophyticus., S. lugdunensis - has many of the virulence factors of S. aureus)- Mainly skin commensals - can be pathogenic in the presence of foreign bodies or immunocompromised
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7
Q

alpha haemolytic streptococci

A

partial haemolysis - Turn blood agar green Streptococcus pneumoniae (pneumococcus) Viridans streptococci

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8
Q

Streptococcus pneumoniae

A

alpha haemolytic pneumonia, meningitis, septicaemia Produces capsule to protect S. pneumoniae from the host so it cant be recognised as foreign

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9
Q

Viridans streptococci

A

○alpha haemolytic ○ Normal oral flora, cause infection in other areasCause of infective endocarditis

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10
Q

beta haemolytic streptococci

A

(complete haemolysis)Turn blood agar clearFurther identified by carbohydrate surface antigens: groups A-G), A,B,D,F clinically most important A. streptococcus pyogenesb. streptococcus agalactiaeD. Enterocossu faecalis, Enterococcus faecium

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11
Q

streptococcus pyogenes

A

group A beta haemolytic major pathogen - pharyngitis, cellulitis, necrotising fasciitis (skin and soft tissue infections, bone and joint infections and can lyse human muscle and connective tissue, can lead to sepsis)

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12
Q

streptococcus agalactiae,

A

group B beta haemolytic neonatal sepsis (meningitis, bacteraemia), genital tract carriage commoninvasive infections in adults often older and underlying factors e.g. diabetes, liver disease/alcohol abuse, CVD, malignancy )

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13
Q

enterococcus

A

group D beta haemolytic often non-haemolytic, enterococcus faecalis found in the gut as normal commensal, cause of UTI and infective endocarditis

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14
Q

classification of gram +ve bacilli

A
  • Aerobic Anaerobic (grow only in the absence of oxygen)spore forming/non-spore forming
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15
Q

classification of gram +ve cocci

A

coagulase test blood agar culture - haemolysis

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16
Q

CLOSTRIDIUM DIFFICILE

A

gram +ve bacilli - Asymptomatic gut carriage in healthy people - Important cause of diarrhoea, associated with toxin production and potentially fatal (toxins found in stool sample)- Increased risk with antibiotic use and anything else that disrupts the normal gut flora - Pseudomembranous colitis - inflammation of the large intestine - Spread/transmitted via spores

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17
Q

CLOSTRIDIUM PERFRINGENS

A
  • gram +ve bacilli Found in soil and normal commensal in human and animal gut/faeces- Spread by spores- Can contaminate food and cause gastroenteritis (enterotoxin producing strains)Infects wounds and can cause gas gangrene
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18
Q

CLOSTRIDIUM TETANI

A
  • gram +ve bacilli - Spread by spores- Toxin produced by C. tetani can produce tetanus ○ Uncontrolled muscle spasm Antigenically modified toxin (toxoid) used for immunisation
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19
Q

colonisation

A

bacteria grow on body sites exposed to the environment, without causing any infection. This is a normal process.

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20
Q

infection

A

presence of microorganisms causing damage to body tissues, usually in the presence of acute inflammation

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21
Q

gram -ve cocci

A

Neisseria meningitidis Neisseria gonorrhoeaeMoraxella catarrhalis

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22
Q

Neisseria meningitidis

A

gram -ve coccus meningitis and septicaemiaimportant when isolated from a sterile site (e.g. blood cultures or CSF, gram staining is very important to identify the bacteria here), PCR available on EDTA blood for N. meningitidis, often life threatening

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23
Q

Neisseria gonorrhoeae

A

gram -ve coccus causes urethritis in men and pelvic inflammatory disease in women, spread by sexual contact, causes gonorrhoea, identical appearance to Neisseria meningitidis on gram stain (differentiate by clinical findings)

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24
Q

Moraxella catarrhalis

A

gram -ve coccus causative agent of respiratory tract infections, especially in those with underlying lung pathology

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25
Q

what are coliforms

A

organisma which are in the family Enterobacteriaceae • Mainly commensals of the human large intestine (gut commensals) • Key example is E. coli Lactose fermentation is a useful preliminary test in classifying gram -ve bacilli (can use selective agar)

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26
Q

ESCHERICHIA COLI

A

-gram -ve bacilli Human and animal reservoirs160 serotypes, strains vary in terms of disease potential - Sexual virulence mechanisms: pili, capsule endotoxin and exotoxins - Major form of food borne infection- Ferments lactose- Important cause of UTI and septicaemia, also neonatal sepsis- enterotoxogenic and enterohaemorrhagicDon’t treat with antiobiotics - these could lead to more toxins being produced

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27
Q

SALMONELLA SPP.

A

-gram -ve bacilli - Major form of food borne infection- DOES NOT ferment lactose - Salmonella enterica: Self-limiting enterocolitis with or without bloody diarrhoea - 2nd commonest cause of bacterial diarrhoae in the UK - Can be invasive i.e. enters bloodstream

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28
Q

SALMONELLA TYPHI

A
  • gram -ve bacilli Distinct from Salmonella enterica- Cause of typhoid fever - Fever, constipation early stagesfatal if untreated- Organism can be isolated from blood cultures as well as faecesRisk during foreign travel but vaccine available
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29
Q

curved gram -ve bacilli

A

Campylobacter sppHelicobacter pylorivibrio spp

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30
Q

Campylobacter spp.

A

curved gram -ve bacilli microaerophilic (likes low oxygen), source is domestic animals and chickens, spread via faecal-oral route, foul smelling –> bloody diarrhoea (incubation period 2-5 days), commonest cause of bacterial diarrhoea in UK , no vaccine currently, often seen in springtime, can enter the bloodstream, not treated with antibiotics unless very severe

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31
Q

Helicobacter pylori:

A

curved gram -ve bacilli natural habitat is human stomach, damages mucosa and causes ulcers, strong risk factor for gastric adenocarcinoma (oncogenic organism), treat to avoid future cancer risk

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32
Q

Haemophilus influenzae

A

gram -ve cocco-bacilli (mixed appearance), causes respiratory tract infection (2y to S, pneumoniae), capsulate for (type b) was formerly an important cause of meningitis in children, other no-typable forms of H. influenzae still able to cause meningitis

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33
Q

Pseudomonas SPP - P. aeruginosa

A

anaerobic gram -ve bacilli-Water and soil coloniser - drains, sinks, mops- May contaminate medical equipment - Can colonise upper resp tract - Hospital acquired cause of sepsis e.g. UTI, bacteraemia, pneumonia (rare)- Feared respiratory pathogen in CF- Multi drug resistance mechanisms Limited treatment options

34
Q

anaerobes

A
  • Often part of polymicrobial infection e.g. liver/brain abscess- Increasing importance and recognition - Bacteroides spp, Prevotella, Porphyromonas- Difficult to grow in the lab due to their sensitivity to oxygen Bacteroides fragilis • Part of normal colonic flora• Causes intra-abdominal abscess• May spread to other sites e.g. blood
35
Q

oral anaerobes

A
  • Prevotella - Porphyromonas e.g. P. gingivalis - Pasteurella spp- Capnocytophyga spp- Important in aetiology of periodontal disease and may be part of polymicrobial dental abscesses- Role in aspiration pneumonia - Human and animal bit infections
36
Q

miscellaneous bacteria

A
  • Not all bacteria can be stained w/ Gram’s method - Not all bacteria can be cultured by standard methodsMycobacterium spp, spirochaetes, chlamydia/chlamydophila
37
Q

acid and alcohol fast bacteria

A

• Resistant to decolourisation by acid or alcohol after staining with carbol fuchsin Mycobacterium species are visualised with special stains e.g. ZN or auramine

38
Q

lab identification of mycobacteria

A

• ZN or auramine phenol screening • Doesn’t identify species • Culture required for ID ○ New automated liquid culture ○ Growth in 2-4 wksMolecules detection and identification of MTB possible

39
Q

tuberculosis

A

• Caused by mycobacterium tuberculosis • Linked with HIV • Recommended rapid diagnostic nucleic acid amplification tests for diagnosing pulmonary (including laryngeal) TB in adults if there is: Clinical suspicion of TB disease and the person has HIV In circumstances in which rapid info about mycobacterial species would alter the person’s care In a situation where a large contact tracing initiative is being exploited

40
Q

Mycobacterium leprae

A

cant be cultured, mainly India, Nepal, Brazil, parts of Africa, attacks peripheral nerves

41
Q

SPIROCHAETES

A

mycobacteria long, spiral shaped bacteria; not easily visualised by light microscopy, very difficult to culture (never Treponema pallidum), dark ground microscopy or immunofluorescence, often diagnosed by serology Common spirochaete diseases: Treponema pallidum (syphilis), Borrelia burgdoferi (lyme disease), Leptospira interrogans (Leptospirosis)

42
Q

SYPHILIS

A

spirochaete treponema pallidum 1y - non-painful skin lesion2y - generalised systemic illness and rash, latent phase - symptomatic episodes may occur3y -CNS, congenital syphilis: stillbirth, neonatal death or disease diagnosis - serology, nucleic acid amplification tests (NAAT), part of antenatal screening, management - antibiotics, contact tracing and screening

43
Q

lyme disease

A

mycobacteria transmitted by ticks, stage 1: skin rash (erythema chronicum migrans) appears at the site of the tick bite, stage 2: systemic illness occurs in some patients, wks/mths later when patients suffer cardiac or neurological and muscoloskeletal symptoms, stage 3: chronic disease, occuring yrs later when patients present with chronic skin, nervous system or joint abnormalities. Diagnosed by clinical assessment and serology (antibody detection)

44
Q

leptospirosis

A

mycobacteria infects animals and concentrates in the kidneys, spread is via urine and other body fluids and tissues (zoonosis), at risk groups (sewage workers, water sports), range of clinical presentations (Weil’s disease: febrile illness with systemic upset, liver and renal failure, aseptic meningitis, 10% mortality)

45
Q

chlamydia

A

obligate intracellular bacteria, cultured only in cell lines, can be diagnosed by serology, respiratory infection (chlamydophila pneumoniae, Chlamydophila psittaci (psittacosis) - contact with birds), ophtalmic and genital tract infectionChlamydia trachomatis: trachoma (tropical eye infections), genital and neonatal infection, diagosis: NAAT on 1st void urine or vulval/vaginal swabs, often asymptomatic in women, can lead to pelvic inflammatory disease and infertility

46
Q

define commensal

A

organism which is part of the normal flora e.g. E. coli in the gut, S. aureus in the nose

47
Q

define pathogen

A

organism which can cause disease

48
Q

what are the requirements for a micro-organism to cause infection

A

infectivity and virulence

49
Q

infectivity

A

ability to become established on or within a host ○ Attachment: E. coli (P-fimbriae, receptor on uroepithelial cells)Acid resistance: Helicobacter pylori - lives in the stomach and causes gastritis and gastric ulcers (urease, makes ammonia from urea)

50
Q

virulence

A

capacity to cause harmful effects (disease) once established ○ Conferred by virulence factors: genetically determined microbial components § Invasiveness, toxin production, evasion of immune system □ INVASIVENESS: Streptococcus pyogenes (Group A streptococci), necrotising fasciitis, cellulitis, connective tissue breakdown (hyaluronidase, collagenase), fibrinolysis (streptokinase)Specific to strains, not species

51
Q

exotoxins

A

released extracellularly by the microorganism

52
Q

enterotoxins

A

exotoxins which act on the GI tract

53
Q

example of an exotoxin

A

e.g. SUPERANTIGENS: Certain exotoxins of S. pyogenes and S. aureus. Able to stimulate division of T cells in the absence of specific antigen. Overwhelming cytokine production causes toxic shock

54
Q

examples of enterotoxins

A

CHOLERA: Vibrio cholera, colonises S intestine, enterotoxin production (increases cAMP levels, inhibits uptake of Na+ and Cl- ions, stimulates secretion of Cl- and HCO3- ions. Passive (massive) outflow of water, causes death by dehydration, treated by rehydration

55
Q

endotoxins

A

structurally part of the gram -ve cell wall

56
Q

examples of endotoxins

A

Lipopolysaccharide (Lipid A, oligosaccharide core, specific polysaccharide chain), E. coli and other gram -ve bacilli, Neisseria meningitidis, induces severe uncontrolled host response (cytokine production, fever, rigors, hypotension, tachycardia, collapse

57
Q

superantigens

A
  • Certain exotoxins of S. pyogenes and S. aureus- Able to stimulate division of T cells in the absence of specific antigen- Overwhelming cytokine production causes toxic shock
58
Q

influenza A

A
  • Virus infects cells of the respiratory tract- Destruction of respiratory epithelium which can lead to secondary bacterial infections- Altered cytokine expression leading to fever• Non-human host for influenza a play a key role in generating new virus types through antigenic shift
59
Q

antigenic drift in influenza A

A

minor changes, in the genes of flu viruses, occurs gradually over time to generate antigenic variantsleads to a generation of novel influenza viruses

60
Q

antigenic shift in influenza A

A

(abrupt major changes in antigenic structure)leads to generation of novel influenza viruses

61
Q

enterovirus infections (5)

A
  • Poliomyelitis (poliovirus)- Aseptic meningitis (many enteroviruses)- Myocarditis (coxsackie B viruses)- Pancreatitis (coxsackie B viruses)Respiratory infections (many enteroviruses)
62
Q

example of a latent virus infection

A

herpes simplex virus - cold sores (type 1) and genital lesions (type 2)

63
Q

virus induced tumours

A
  • E.g. papillomaviruses - cervical carcinoma, Retroviruses - lymphomas and leukaemiasHuman T - lymphotropic virus 1 (HTLV-1): transmission by blood and mother to child, infects T cells, modifies host cell gene expression using a transactivating protein, variety of diseases including leukaemia (adult T cell lymphoma-leukaemia), directly responsible for the tumour
64
Q

active immunisation

A

natural/artificialantigen stimulates immune responselong term immunity immunological memory no immediate effect but faster and better response to next antigenic encounter

65
Q

live attenuated vaccine

A

attenuation of a pathogenic organism by repeated passage in cell culture or non-human hostusually promote a full, long-lasting antibody response after one or two dosesreversion to wild-type organism may occur contraindicated in some individualsrequire refrigeration until administration

66
Q

killed vaccine

A

inactivated pathogenic organism reversion to wild type organism doesnt occur promote weaker immune responses in comparison to live vaccines - multiple doses may be requiredsome inactivated vaccines contain adjuvants possible side effects of producing inflammatory responses

67
Q

adjuvants

A

substances that enhance the antibody response

68
Q

examples of attenuated vaccine

A

MMR, BCG, polio, varicella zosterm, yellow fever

69
Q

examples of killed vaccines

A

polio, hep A, rabies

70
Q

toxoid vaccine

A

toxin treated with formalintoxin retains antigenicity but has no toxic activity only induces immunity against the toxin and not the organism that produced it

71
Q

examples of toxoid vaccine

A

tetanus, diphtheria

72
Q

define latent infection

A

type of infection that may occur after an acute episode; the organism is present but symptoms are not; after time the disease can reappear

73
Q

define asymptomatic infection

A

patient is a carrier for a disease or infection but experiences no symptoms

74
Q

host defence mechanisms

A

innate and acquired immunity phagocytosis antibodies and complement cell mediated immunity

75
Q

innate immunity

A

physical defencesphagocytic cells

76
Q

acquired immunity

A

specific response to antigen leads to immunological memory humoral and cellular

77
Q

phagocytosis

A

polymorphs (neutrophils, eosinophils, basophils) and monocytes in bloodmononuclear phagocytic system: spleen, liver and regional lymph nodesother white cells

78
Q

antibody and complement

A

involves immunoglobulinsneutralised toxin, neutralised virus, prevents adherence of microorganisms, opsonises capsulate organisms, useful in diagnosis humoral immunity: mostly bacterial infection, extra-cellular, acute inflammation, neutrophilia

79
Q

cell mediated immunity

A

combat intracellular infectionmacrophages present antigen and stimulate T cells, cytokines produced and control the response

80
Q

enterotoxogeic E coli

A

commonest cause of traveller’s diarrhoea (contaminated water)

81
Q
  • Enterohaemorrhagic E. coli
A

more severe form, bloody diarrhoea, haemolytic uraemic syndrome (HUS) associated w/ E. coli O157

82
Q

shigella

A

not lactose fermenting low infective dosefaecal-oral spreadbacillary dysentery some strains produce toxin4 species