Becky Wright - bacteria Flashcards

(88 cards)

1
Q

Describe the Gram-staining process steps and outcomes:

A

Heat fixed cells

1) Crystal violet (violet gram positive)
2) Iodide added (binds to Crystal violet and traps large complexes in gram positive cells)
3) Ethyl alcohol (decolourises gram negative, removing its outer lipopolysaccharide layer, exposing thin peptidoglycan layer, which liberates CV-I complexes)
4) Safranin counterstain (pink for gram negative)

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2
Q

Blood agar, chocolate agar. What are they and what’s the difference?

A

Enriched nutrient agars,

Chocolate agar’s blood cells are heated to lyse them, allowing the growth of fastidious (picky) respiratory bacteria like Haemophilus influenzae and Neisseria meningitidis

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3
Q

How might you differentiate Staphylococcus aureus from other aerobic gram positive bacteria using 2 tests?

(any other tests?)

A

Catalase positive (vs Streptococci)

Coagulase positive (vs other Staphylococci species)

[MSA selective medium: salt and mannitol **fermentation **–> yellow]

[haemolytic –> golden cluster colonies on blood agar]

[DNAase positive, clears around colonies]

POSITIVE FOR EVERYTHING

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4
Q

3 Skin infections caused by Staph.aureus?

(a gram positive coccus)

A

Furunculosis/Folliculitis (boils)

Impetigo (rupturing pustules –> crusty, infectious)

Cellulitis (subcutaneous tissue infection)

NOT necrotising fasciitis (Strep pyogenes does that)

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5
Q

Describe some of the virulence factors of Staphylococcus aureus:

A

Adhesion factors: variety of MSCRAMMS

Enzymes: Lipases etc digest host tissue, coagulase forms fibrin coat

Protein A: binds Ab Fc portion

Exotoxin: PVL often in MRSA

Exotoxins: Staphylococcus Enterotoxins, SEs (A-E,G-J)

Exotoxin: TSST-1 Superantigen (toxic shock syndrome)

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6
Q

Streptococcus pyogenes classification methods?

A

Gram positive cocci (in chains)

Grown on blood agar (won’t grow on nutrient agar like Staph.aureus can) **Beta-haemolytic **yellow colonies

Catalase negative (unlike S.aureus)

Lancefield group A (Group A strep) (antibodies to specific group carbohydrates in the cell walls)

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7
Q

Diseases caused by Streptococcus pyogenes?

A

Skin/soft tissue infections like Impetigo, Cellulitis, Necrotising fasciitis

Strep. throat, tonsilitis, Scarlet fever (rash and fever typically in children)

Toxic shock syndrome, bacteraemias etc..

Noninfectious sequelae like Rheumatic fever or acute glomerulonephritis

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8
Q

Streptococcus pyogenes virulence factors?

A

Adhesion factors: Surface F protein. Lipoteichoic acid LTA (a Gram +ve cell wall component) binds fibronectin.

_Immune evasion: _**M protein **(variable) binds host proteins, destabilises complement, bind fibrinogen (activating neutrophils)

Poorly immunogenic capsule.

C5a peptidase degrades complement.

Enzymes: **Streptokinase! **Fibrinolytic. Activates plasminogen.

Hyaluronidase (digests ECM component, carbon source and invasion?)

_Exotoxins: _**Pyrogenic, **strain specific, SPE: A/B/C

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9
Q

Non-infectious sequelae of Streptococcus pyogenes infection?

A

Autoimmune damage mediated:

Rheumatic fever: Joint and heart valve inflammation and damage. Normally associated with pharyngitis and specific M proteins.

Acute glomerulonephritis AGN: Different strain

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10
Q

Define diarrhoea, dysentery, food poisoning, and gastroenteritis:

A

Diarrhoea = change in frequency or consistency of stools

Dysentery = blood and mucus in faeces (from inflammation), diarrhoea, abdominal pain

**Gastroenteritis = **nausea, vomiting, diarrhoea

Food poisoning = gastroenteritis symptoms associated with a particular food source

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11
Q

What is MacConkey agar?

and what is SMAC for?

A

MacConkey agar is selective agar for gram negative bacteria (such as E.coli)

It contains bile salts to inhibit Gram positives, and neutral red pH indicator that turns pink if colony ferments lactose

[Sorbitol MacConkey agar is selective for enteropathogenic E.coli strain O157:H7. Lactose replaced with sorbitol. Salmonella and shigellas can’t ferment lactose, and this pathogenic strain of E.coli can’t ferment sorbitol (unlike other non-pathogenic strains)–> colourless colonies.]

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12
Q

What are serotypes? serogroups?

(pathotypes and strains?)

A

The serotypes of bacterial cells are their classification by different surface antigens. Serogroups are groups of serotypes with some of the same antigens.

Strains can be often recognised by their serotypes.

Different pathotypes cause different patterns of infections because they produce different virulence factors. Specific serotypes can be associated with specific syndromes.

(EHEC pathotype often has serotype: O157:H7 associated with HUS)

O = somatic, cross species. H = flagellar antigen, more specific

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13
Q

Enterotoxigenic ET E.coli?

Pathophysiology and symptoms

A

Causes travellers diarrhoea (ET was a traveller?)

Virulence factors: Adhesins = colonisation factor antigens (CFAs)

Enterotoxins –> diarrhoea

Heat-stable toxin (ST) –> cGMP –> fluid secretion

Heat-labile toxin (LT) –> cAMP –> chloride and fluid secretion

(stable like the Ground, labile like the Air)

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14
Q

Enteropathogenic, EP, E.coli, EPEC?

Pathophysiology and symptoms?

A

Diarrhoea in children under 2yo!

  • Pathogenicity island contains LEE (locus for enterocyte effacement)
  • Encodes a Type III secretion system T3SS/injectosome!
  • A needle-like structure that inserts Tir into host cell
  • Intimin binds Tir (attachment)
  • Causes diarrhoea by effacement of microvilli, effacing lesion caused by attachment
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15
Q

Enterohaemorrhagic E.coli EHEC? (and STEC, VTEC)

Pathophysiology and Symptoms?

Source of infection, reservoir?

A

Commonly serotype O157:H7

Different names: STEC =shiga-like toxin producing e.coli

VTEC = verocytotoxin (shiga-like) producing e.coli

Can lead to bloody diarrhoea and even HUS

Adhesion like EPEC.

Toxins encoded by bacteriophage Stx phage.

Release caused by phage mediated lysis in response to stress! therefore don’t treat with Abx

Source of infection = contaminated food

Reservoir = cattle

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16
Q

Shiga toxin Stx, mode of action?

A

Binds Globotriaosylceramides Gb3s

on Paneth (goblet) cells in intestine, and kidney epithelial cells.

Inhibit protein synthesis by disrupting ribosomes

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17
Q

What is special about EaggEC in the german outbreak?

A

Serotype O104:H4

EaggEC with shiga toxin producing capability.

Higher number of cases of HUS, possibly due to better adhesion (aggregation of cells on top of each other) and so better uptake of toxin?

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18
Q

How to screen and diagnose EHEC?

A

[Diarrhoea only diagnosed when severe, persistant or with HUS]

SMAC (sorbitol-MacConkey agar) colourless colonies (non-sorbitol fermenting, unlike normal flora)

Follow up this screen with PCR for shiga-like toxin and serotyping (serology)

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19
Q

Common causes of travellers diarrhoea?

A

ETEC and EAggEC most cases but typically not diagnosed

Most diagnosed cases are Salmonella, Shigella and Campylobacter

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20
Q

Compare and Contrast E.coli and Salmonella:

A

Both** **Gram negative bacilli, facultative anaerobes that grow on unenriched media

Both oxidase negative

Both possess O and H antigens

But: E.coli ferments lactose whilst salmonella doesn’t

Salmonella produces H2S (hydrogen sulfide)

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21
Q

4 Salmonella *enterica *subspecies and their 2 diseases:

A

Salmonella Typhi and Paratyphi cause Enteric/Typhoid fever

Salmonella Typhimurium and Enteritidis cause gastroenteritis

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22
Q

Salmonella gastroenteritis epidemiology and pathophysiology?

A

Reservoir: GI tracts of birds (poultry), domestic animals, reptiles

Source of infection: heavily contaminated food, esp. poultry

Pathophys: Attachment by T3SS in small intestine

Triggers endocytosis, multiplies in vesicle, kills host cell inducing fever, pain and diarrhoea

TLR4 recognition –>cytokines–>neutrophil migration

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23
Q

Salmonella *enterica *Typhoid fever (Typhi or Paratyphi)

Epidemiology and Pathophysiology?

A

Epidemiology: Reservoir = human, case or carrier (e.g. in gall bladder intracellular or gallstone biofilm)

Source of infection mode of transmission: ingestion of contaminated food

Pathophysiology: SPI7 (salmonella pathogenecity island 7) Helps export of Vi capsular antigen, capsule –> evades TLR4

SPI7 Encodes Tvi regulatory protein that inhibits flagellin, normally recognised by TLR5 –> evades

Enters macrophages –> lymph nodes –> blood –> liver,spleen,BM,gall bladder –>blood –>other tissues

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24
Q

Contrast management of Salmonella Typhi and Typhimurium: Typhoid fever vs gastoenteritis

A

Typhoid fever –> blood sample. Abx. Quarantine. Source control. Gall bladder removal in carriers?

Gastroenteritis –> stool sample. no Abx (self-limiting), source control

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25
Shigella vs Salmonella
Both gram-negative bacilli Both non-lactose fermenters (unlike E.coli) Shigella doesn't produce H2S like Salmonella
26
Shigella *dysenteriae* epidemiology and pathophysiology?
Travel associated, and paediatric, transmitted by faeco-oral route, unwashed hands on food? Pathogenesis: **Infects M cells of intestine**, spreads to surround epithelial cells, **causes abscesses** as cells killed Can cause HUS with Stx. Dysentery = Blood mucus stools, abdo pain --\> Abx if severe/extreme ages
27
Vibrio cholerae shape vs E.coli? What pathotype of E.coli is Vibrio cholera like?
Gram negative bacilli but comma-shaped Vibrio = Monotrichous flagellum Like Enterotoxic ETEC, cholera toxin increases cAMP, like heat-labile toxin, LT Cholera reservoirs = water and people
28
Campylobacter *jejuni *source and symptoms?
Animal faeces source e.g. poultry Symptoms like gastroenteritis or dysentery
29
List different types of UTI and their features:
Lower UTI, cystitis or urethritis (dysuria, lower abdo pain, increased frequency) Upper UTI, **Pyelonephritis **or urethritis (pyelonephritis kidney damage, sepsis, fever chills and rigor, flank pain, nausea vomiting)
30
How can E.coli, or other gram negative bacteria cause sepsis?
Gram negative cell wall contains **LPS (lipopolysaccharide) endotoxin** LPS released upon lysis, bound to **LPS-binding-protein. LBP** **LBP** binds PRRs **CD14 and TLR-4** receptor complex on **macrophages.** Binding causes intracellular activation of **nuclear factor kappa beta** Causes release of cytokines --\> shock
31
Physical host defences againt urinary tract infection?
Urine flow _Antibacterial properties of urine:_ High osmolarity High urea content Sphincters Epithelial barrier
32
Normal flora of the urethra? commonly contaminates urine samples
Diphtheroids Streptococci Lactobacilli and Gram negative bacilli in women
33
Common virulence factors of UPEC? uropathogenic E.coli
_Adhesins:_ **(Type1 and P-) Fimbriae** adhere to urinary epithelial cell receptors: Type-1 fimbriae to **Mannosides in bladder** and P-fimbriae to **Glycosphingolipids in kidneys** respectively _Toxin:_ **a-Haemolysin** lyses RBCs (helps spread) Gram neg capsule prevents phagocytosis **Siderophores** such as **Aerobactin** collect **iron**
34
Innate immune response to adherence of bacteria (of UPEC in kidney)?
In renal tubule epithelial cells: UPEC bacteria bind using their **P-fimbriae to glycosphingolipids** Sensed by **TLR-4**, a PRR, which causes release of **chemokine IL-8** Binds **CXCR1** (chemokine receptor 1) on **neutrophils** and on renal **epithelial cells**! **Recruits neutrophils** and causes their **migration across epithelium.**
35
3 Gram negative, oxidase negative bacilli that commonly cause UTI?
Escherichia *coli* (causes up to 90%) Proteus mirabilis Klebsiella pneumoniae
36
Features of Proteus mirabilis (UTI causing agent):
Strong **urease** activity (as seen on blood agar) Cleaves urea to ammonia --\> alkaline urine **Alkaline urine --\> KIDNEY STONES**
37
Enterococcus faecalis key features (for UTIs)
Gram positive cocci, catalase negative Acquired typically from hospital equiment like cystoscopes.
38
Pseudomonas *aeruginosa* key features:
Gram negative bacilli, [oxidase positive unlike UPEC]. **Makes blue green fluorescent colonies**. Opportunistic typically nosocomial pathogen infects immunocompromised patients, patients with catheters or vesicoureteral reflux. Often contaminates hospital water supply!
39
Which organism can cause descending UTI?
Staphylococcus *aureus*
40
Demographic factors in UTI?
E.coli UTI --\> Mostly young women after sexual activity. Also in children (perhaps vesicoureteral reflux or poor hygiene) Elderly men (prostatic enlargment) Uncommon in young men.
41
What do pus cells, epithelial cells, casts, and crystals each signify in urine microscopy?
Pus cells (neutrophils) suggest infection Epithelial cells suggest contamination Casts suggest kidney pathology Crystals suggest underlying abnormality (maybe fragments of a kidney stone?)
42
Key considerations in urine culture:
Semi-quantitative culturing: 100,000 colony forming units per ml is cut off (100/µl) CLED (cystine, lactose, electrolyte deficient) agar is common medium to differentiate between organisms Bromothymol Blue indicator Yellow = lactose fermenting (like E.coli) Electrolyte deficiency prevents Proteus 'swarming'
43
4 Common causes of bacterial meningitis:
**Neisseria meningitidis** (gram -ve cocci, oxidase +ve) AKA "meningococcus" (capsule serogroups A,B,C (B most common as vaccine only recently created) **Streptococcus pneumoniae** (gram +ve cocci) **Haemophilus influenzae** (gram -ve bacilli) type B (HIB vaccine) **Listeria monocytogenes**
44
Neisseria meningitidis (gram -ve coccus) reservoir, transmission, infection? symptoms/signs?
**Human nasopharynx** only reservoir of N.meningitidis. Spread through close contact, overcrowding. Enters blood stream (septicaemia --\> non-blanching rash) --\> CSF Or straight to CSF through cribiform plate/olfactory nerve (meningitis: stiff neck, photophobia, severe headaches)
45
Neisseria meningitidis (gram neg coccus) virulence factors?
**(Type IV) Pili twitch** --\> move through **mucus** **Capsule** (makes C3b opsonin inaccessible to WBCs) **LOS** (small version of LPS, endotoxin --\>haemolysis, DIC (activates coagulation) and sepsis via TLR4) Coats self in **non-immunogenic** host **Sialic acid** **Ig A protease** digests IgA! Complement inhibitor (fHbp) **Survives ROS attack inside neutrophils** --\> hides in them
46
4 Physical defences against LRTI (e.g. pneumonia)?
**_Mucociliary escalator_**: Mucus (trap bacteria) Cilia (beat in coordinated waves) + Mucous membranes + Lysozyme (attacks peptidoglycans, esp. in Gram pos cell wall)
47
5 Risk factors for pneumonia?
Extremes of **age** (2 or under or 65+) Chronic lung disease (**asthma, COPD**) **Smoking** **Hospitalisation** (nosocomial infection) **Immunosuppression** (HIV, steroids etc)
48
4 causal agents of pneumonia? common? atypical?
**Viruses** like RSV (children) **Strepococcus pneumoniae** (commonest bacterial) Atypical (**Legionella pneumophila, Mycoplasma pneumoniae**)
49
Typical symptoms of pneumonia?
Cough (productive) and Dyspnoea High Fever, Fatigue, Myalgia
50
Streptococcus *pneumoniae* infection: | (alpha haemolytic, optochin sensitive)
**Colonises nasopharynx**, aspirated into lungs, requires weak immune response or structural problem to survive **Capsule** poorly immunogenic and resists phagocytosis, but is basis for pneumococcal vaccine. Can lead to **septicaemia** in immunocompromised persons Can lead to **meningitis in children**
51
How to diagnose pneumonia? Particularly Streptococcus pneumoniae?
Symptoms important. Sputum culture is problematic as Strep. pneumoniae are normal commensals of pharynx, **contamination**. **Alpha haemolytic** gram pos cocci, **optochin sensitivity** differentiates from harmless Strep.viridans. (see pic)
52
Atypical pneumonia symptoms, agents, problems?
Non-specific symptoms (headache, malaise, myalgia, nausea), typically don't seem severe (walking pneumonia) Legionella pneumophila (caught from water or soil) Mycoplasma pneumoniae (no peptidoglycan --\> Resists Abx, intracellular) **Recquire different ABx, and hard to culture** (fastidious)
53
Legionella *pneumophila* (gram negative (stains poorly) rod): Source and Intracellular replication (in Macrophages)
Contaminated water supplies cause local outbreaks Evades lysosome fusion after phagocytosis, creates its own ER-like vesicle Replicates to high numbers and lyses cell.
54
Define minimal inhibitory concentration testing, MIC (of Abx):
**Lowest concentration of antimicrobial that inhibits visible growth of a microorganism after incubation** (gives a guide on whether resistant and how much needed, MIC in tubes is cumbersome --\> use disk diffusion testing)
55
What are breakpoints? (in disk diffusion susceptiblity testing or MIC)
Cut-off points published by **BSAC** defining at what diameter **zone of inhibition** or MIC a bacteria is considered resistant or susceptible (or indeterminate). Depends on type of bacteria, type of antibiotic and even sometimes type of infection (location etc)
56
What are Macfarland standards?
A method for **internal quality control** in antimicrobial susceptibility testing. Standard suspensions representing **opacity** of different concentration bacterial suspensions, used for **comparison to standardise innoculum density for MIC.**
57
Mueller-hinton agar?
Used for **disk diffusion antimicrobial susceptibility testing.** (loose agar --\> better ABx diffusion) (contains starch, which neutralises toxins that could otherwise interfere with Abx)
58
What is NEQAS?
**National external quality assessment service.** **External quality control** for microbial laboratories, for example antimicrobial susceptibility testing. Samples and results sent for assessment regularly.
59
Clostridium species characteristics?
**Anaerobic, gram positive bacilli!** **Spore forming **(survival under harsh conditions) Vegetative cells produce various **exotoxins**
60
Clostridium tetani: Reservoir, transmission, toxins?
Found in **soil, dust, and intestinal tracts** of animals and humans. Infects **wounds** directly, needs **anaerobic environment** e.g. deep wounds. Produces **tetanospasmin** and tetanolysin toxins.
61
**Tetanospasmin** method of action
2 heavy chains: Heavy chain binds to **gangliosides** on peripheral neuron terminal and **endocytosed** **Retrograde axonal transport to CNS** Enters **inhibitory** neurons in CNS Light chain released and **cleaves synaptobrevin,** a SNARE protein (involved in neurotransmitter release) Therefore BLOCKS INHIBITORY SIGNALS!
62
Typical tetanus cases and symptoms?
**Wound infection** in unimmunised person. **Neonatal tetanus** from umbilical stump infection. (unimmunised mother and unsanitised conditions) **Maternal tetanus** following childbirth Symptoms: muscle spasm (lock jaw, respiratory muscle spasm leads to death)
63
Tetanus vaccine?
A **toxoid**: toxin extracted from culture and inactivated by formaldehyde. Toxoid triggers primary immune response --\> memory cells. Immunity.
64
Clostridium botulinum: source and symptoms? (Gram positive spore-forming bacillus)
**Soil, contaminated food** (ingestion of toxin), **wound infection** (e.g. IV drug users), **Infant botulism** most common, normal gut flora not well established and bile acids low. Botulism: Blurred vision, drooping eyelids, paralysis of various muscles (potentially fatal)
65
Botulinum toxin mechanism of action? Treatment?
Enters blood stream to spread throughout body. **Blocks ACh release at NMJ -**-\> paralysis. **Blocks** **SNARE protein SNAP 25** (so vesicles cannot fuse) Antitoxin (antibodies against toxin given)
66
Clostridium difficile, symptoms and mode of infection? Complications?
* **Diarrhoea upon toxin production,** abdo pain, fever, raised WBC, blood in stools? * **Resides in human gut, **asymptomatic carriage without toxin, associated with **ABx treatment** reducing competing flora (opportunistic) _Complications_ include **Pseudomembranous colitis** in severe cases and **recurrence** due to persistant spores.
67
C.difficile toxins A and B, method of action?
Toxin A, TcdA, enterotoxin binds apical side. Endocytosed, cytotoxic, cells lose structure because reduces F-actin --\> opens tight junctions between cells. Recruits neutrophils Toxin B, TcdB, cytotoxin binds basolateral side (through opened tight junction?) Recruits neutrophils.
68
Diagnosis and Treatment of C.difficile?
_Diagnosis: _**Stool sample,** **detect toxins A and B with ELISA. Or PCR for toxin genes.** Culture and testing for cytopathic (toxin) effects on cell lines is slow but gold standard for confirmation. _Treatment:_ Stop original Abx, start anti Cdiff ABx. Infection spread control (isolation, decontamination, handwashing), faecal transplants?
69
How are species of mycobacterium stained and further classified?
**They are acid fast,** (when stained with Carbol fuschin, appear **red, not-decolourised by acid**, methylene blue counterstain background) _Further classified_ into '**fast**' and '**slow**' growing, fast are typically harmless environmental, slow include M.tuberculosis and M.bovis, **culture takes weeks**!!
70
What is mycolic acid? and what is it responsible for?
**Waxy coat** present in the cell wall of mycobacteria. It enhances the hardiness and pathogenicity of the mycobacteria, by resisting common Abx and digestion within macrophages. Also accounts for poor staining with gram's. (hence acid fast staining used)
71
Problems with diagnosis of mycobacterial infection?
**Acid fast staining of samples (e.g. sputum) has high false negative rate.** (low sensitivity) Symptoms non-specific **Culture is SLOW.** Risk to lab tech, need level 3 containment.
72
TB as an obligate pathogen?
When TB bacilli present they are never normal flora, always pathogenic. Therefore it is a latent infection. However it is different from active TB disease, which requires symptoms and signs. Chronic disease associated with chronic inflammation.
73
Worldwide burden of TB, stats:
1/3rd of worlds pop infected. 5-10% of those infected will develop active disease. Often associated with HIV, more likely to develop disease
74
Reservoir and mode of transmission of TB?
I**nfected humans are main reservoir** (rarely cattle) **Positive smear** (for acid-fast bacilli) means **more infectious**. Mode of transmission is inhalation, increased by crowding, close contact. Possible genetic susceptibility?
75
Stages of TB infection pathogenesis?
1. Engulfed by macrophages, but survive due to waxy coat (mycolic acid) and **serine protease** that helps maintain a normal pH, 2. Macrophages and activated T-cells keep infection localised to **primary lesion** in lung. Consisting of activated giant epitheloid macrophage cells. 3. Primary complex = lesion and enlarged hilar lymph nodes. Lesion sometimes becomes necrotic, caseous. 4. In latent stage lesion is sealed off by fibroblasts. Sometimes becomes calcified. 5. Occassionally dissemination could lead to miliary TB, or more commonly reactivation in immunosuppressed (e.g. older) patients
76
Pathogenesis of TB disease through reactivation or dissemination?
From reactivation of dormant bacteria, increasing cavitation occurs, this is common in patients with lowered immunity. If this cavity communicates with an airway sputum is contaminated and the person is infectious. In rare cases of severe immunocompromise (e.g. in HIV) spread can occur by bloodstream (miliary TB)
77
Only way to diagnose latent TB infection (not active disease)?
Tuberculin skin test, against TB antigen (Mantoux test) (won't be acid-fast bacilli in sputum until reactivation) or PCR, new test, can also diagnose Rifampicin resistant
78
2 symptomatic categories of STD?
_Discharge and infertility_: Chlamydia trachomatis Neisseria Gonorrhoea _Ulcerating_: Herpes Syphilis (Treponema pallidum Pallidum)
79
Treponema pallidum pallidum infection, reservoir/source of infection, mode of transmission?
Oligate human parasite, transmission either by **sexual contact** (through mucous membranes, intact or abraded) Or **mother to child** in labour or in utero.
80
3/4 stages of syphilis?
Primary stage = **chancre** after 3 wk incubation (single painless ulcer, on genitals, mouth, anus) INFECTIOUS (promotes HIV transmission too) Secondary stage = **bloodstream** (2-12 weeks later) --\> **Fever**, **rash** (not itchy, palms, soles, elsewhere, widespread) myalgia etc. V.INFECTIOUS Latent stage: less infectious, asymptomatic (years), typically final stage **Tertiary syphilis is rare with treatment: Neurosyphilis,** skin/bone/liver/other **lesions**, cardiovascular syphilis (**aortitis**), can be fatal.
81
Features of congenital syphilis?
Infected mother to foetus, or during birth. (therefore **screen all pregnant women**!) Many foetuses infected early will be **stillborn**. Can cause: Developmental delay, seizures, deformities, hepatosplenomegaly etc. death? Characteristic symptoms, like syphilitic rhinitis, deafness etc..
82
Problems diagnosing syphilis? problem with DFA testing? problem with antibody assays, RPR and TPHA?
Syphilis is delicate, obligate human parasite: cannot be cultured! **Dark field microscopy** (with silver stain) or **DFA** (direct fluorescent antibody) testing involves visualising Treponema pallidum Pallidum within 10 minutes of sample collection and such **specialist equipment is rarely available** (test not sensitive, but very specific) **Antibody testing doesn't work in lag period** before antibodies have been generated.
83
Describe Rapid plasma reagin test for syphilis?
Cheap, sensitive, non-specific screen: Tests for antibodies against common bacterial lipid, **Cardiolipin.** **Antigen bound to carbon particles, to visualise _agglutination_ reaction if antibody present.**
84
Describe TPHA (Treponema Pallidum Haemagglutination assay)?
**Expensive Specific test for antibodies** against specific treponemal antigen. Antigen in kits **bound to RBCs!** --\> Visible **diffuse clumping** if antibody present in patient serum. (negative is small dark button)
85
Treatment and prevention of syphilis? simple
1) Abx (Benzathine Penicillin) 2) Treat partners too! 3) Prevention with safe sex.
86
Characteristics and 2 forms of chlamydia trachomatis?
**Gram** **negative**, **obligate intracellular** bacterium (either shape!) 2 forms: **Elementary** (spore-like) form, infects cells. [infective, metabolically inactive] **Reticular** (vegetative form) intracellular (replicate in inclusion bodies) [non-infective, metabolically active]
87
Clinical features of Chlamydia trachomatis urogenital infection?
Often silent, asymptomatic (50% men, 75% women) Or urethritis, discharge. Women: can lead to PID: pelvic inflammatory disease can lead to infertility. Men: Epididymo-orchitis: pain, swelling etc
88
Best method for diagnosing chlamydia? and national screening program details?
**NAAT** nucleic acid amplification tests (e.g. **PCR**) **detect chlamydial DNA from cervical swabs or urine.** Screening offered to all young people from 2003, as chlamydia common, silent, treatable with ABx.