Bacteria Flashcards

(47 cards)

1
Q

What causes syphilus?

A

spirochete called treponema pallidum

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2
Q

How to syphilus transmitted?

A

transplacentally (mother to child) or sexually

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3
Q

Give the 3 stages of syphilus

A

primary, secondary and tertiary

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4
Q

What can congenital syphilus result in?

A

Miscarriage, stillbirth, congenital malformations

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5
Q

most common site for syphilus to occur? NB mcq

A

anogenital region

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6
Q

Primary syphilus: give the pathogenesis

A
  • Ulcer known as chancre (painless and 3-90 days after exposure occurs)
  • Heals within 3-8weeks and you get regional lymphadenopathy
  • Treponema invade lymph nodes and spread via lymphatics
  • Only see secondary syphilus once the organism is spread throughout the body.
  • Chancre starts as small papule then gets bigger and uclerates
  • ANOGENITAL region is most common NB MCQ!
  • Oral cavity most common extra-genital site!
  • The cancre looks like SSC so include that in differential!
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7
Q

Give pathogenesis of secondary syphilus:

A

-Disseminated disease!! systemic symptoms
-4-10weeks after primary syphilus (primary pyphilus needs to spread through the body first before secondary syphilus occurs)
-Resolves after 3-12weeks
-Not specific symptoms (malais, fever, fatigue) but very characteristic oral lesions coming up!)
-skin rash occurs
-30% oral mucosal mucous patches which fuse and create snailtrack lesions!
-Not ulcer though because ulcer involves full loss thickness epithelium.
-Conylomata lata (frequently anogenital). Do not confuse with conyloma acuminatum caused by HPV! prof van heerden likes to confuse you with this one!
NB test Q is explain or describe the oral manifestations f secondary pyphilus

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8
Q

What occurs in secondary syphilus in HIV patients?

A
  • Chancre change is much bigger (lues maligna explosive and aggressive but is not malignant but looks like malignancy!) was a true and flase Q.
  • Necrotic ulcers of face and scalp
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9
Q

IF you did not know the patient had syphilus and you see the condylomata lata, what does would you suspect in your differential?

A

Differential: 1) patient has HPV and on ARTS because of multiple squamous cell papillomas. 2) patient has hecks disease
3) syphilus (secondary)

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10
Q

Pathogenesis of tertiary syphilus:

A
  • After secondary syphilus , latency of 1-30years. Free of lesions and symptoms.
  • 30% of patients progress to tertiary.
  • Tertiary stage of syphilus is life threatening.
  • CVS and CNS involvement See characteristic lesions that are gummatous necrosis (gumma). Granulomatous inflammation occurs. Gummatous necrosis - syphilitic gumma (patient says his/her palate fell out).
  • Syphilitic gumma causes midline palatal destruction, perforates into nasal cavity. NB test and exam question they looooove this part!.
  • CVS (cardiovascular system): d2 endarteritis of blood vessels. Complications are: end arteries inflammed and occlude.
  • Main 4 CVS issues are: 1. aortic aneurysms (weakening of wall of aorta), 2. left ventricular hypertrophy, 3. aortic valve insufficiency, 4. Congestive heart failure.
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11
Q

CNS problems with teriary syphilus are?

A
  • tabes dorasalis (lose corrdination of movement)
  • Generalised paralysis
  • psyhosis and dementia
  • paresis
  • death
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12
Q

Give the additional features of tertiary syphilus:

A
  • Ocular involvement
  • foci of granulomatous inflammation- gummas
  • palatal gummas perforate into nasal cavity (midline destruction of palatal destruction)
  • atrophy and of tongue papillae = glossitis
  • Nice question to ask final exam all the causes of midline palatal destruction= include gummas in tertiary syphilus.
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13
Q

Congenital syphilus give the 3 pathogonomic features (they love asking this shit)

A

Spirochaetes are around and in tooth germs as teeth develop!
1. hutchinsons teeth (hutchinsons incisors and mulberry molars)
2. oular interstitial keratitis (causes blindness)
3. Deafness (CN 8)
These 3 are also known as hutchinsons triad! NB NB
They give you a picture of hutchinsons incisors and ask what are other features you will find

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14
Q

In addition to hutchinsons triad what other features will you find in these patients with congenital syphilus?

A

Saddle nose deformity, high arched palate, frontal blossing, hydrocephalus, intellectual disability, gummas, neurosyphilus.

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15
Q

You are given a picture of hutchinsons incisors and asked to describe this picture features and other features that will likely be found. Describe (i know there is no picture but you should be able to give a desciption of this)

A
  • Hutchinson incisors show their greatest mesiodistal width in middle third of the crown. The incisal third tapers to incisal edge. This results in resembling a straight edge screwdriver. Incisal edge exhibits a central hypoplastic notch that looks U shaped inwards towards the cervical area.
  • mulberry molars taper towards the occlusal surface with a constricted grinding surface. The occlusal anatomy is abnormal with numerous disorganised globular projections. resembling a mulbery molar on the surface
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16
Q

Give 3 special investigations to diagnose syphilus

A
  1. Active lesions (like chancre or mucous patch) take a smear and do darkfield microscopy which highlights the spirochetes.
  2. iF found positive then want to see if treponema pallidum- do IMF (immunofluorescent) antibody test on the smears
  3. serology
  4. also do warthin starry stain for syphilus
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17
Q

Management and prognosis of syphilus:

A

Penecillin (dosage varies with stage, CNS involvement and immune status)
Use doxycycline if pt is allergic (also tetracycline(NEVER TETRACYCLINE TO CHILD)- TOOTH STAINING), erythromycin, ceftriaxone)

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18
Q

What is the main organism that causes TB?

A

Mycobacterium tuberculosis

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19
Q

How do we distinguish between infection and active disease of TB?

A

TB skin test used! they inject it into skin and if you exposed to it your body will have antibodies against it and your cells will respond to antigen.

20
Q

Explain primary TB

A

-previously exposed
-spread by resp droplets to lungs
If immune system is down then will get TB because bacteria are then freed basically.
In healthy patients granulomatous inflammation surrounds the TB bacilli. Then you asymptomatic. Bacilli remain dormant. Intact immune system prevents disease (as long as you have competent immune system you should not get reactiviation.)

21
Q

Secondary TB explain

A

If you are immunocompromised in ANY way then these organisms will lead to what we call 2ndary TB.
Immunocompromised is eg: child with HIV exposed to TB for first time.
The dormant bacilli reactivate when immunocompromised but most o time occurs when patient is re-exposed to TB when their immunity is down
-5 to 10% occurs later in lie. d2 immunosupression, immune system prevents replication of dormant bacilli.

22
Q

Give 3 predisposing factors of TB

A
  • HIV/AIDS
  • old age
  • diabetes
  • immunisupressed medication (cyclosporine due to organ transplant or cortisone)
  • social factors (poverty and crowding)
23
Q

Give the consequences of TB infection NB will be asked- If a patient has active TB what could be the consequences of infection?

A
  1. Bronchial erosion- cough up sputum (filled with bacilli). They then re-infect themselves at other sites oral lesions. Can also get GIT lesions (when swallow sputum). Also how you get TB ulcer on the tongue.
  2. Pulmonary artery erosion (if the lesion erodes into the pulmonary artery)- infective material circulates back into lung so pt refinecting self. then get widespread lung involvement!!!
  3. pulmonary vein erosion: if the lesion erodes into the pulponary vein to left side of heart to haematogenous spread via aorta- called military TB
  4. lymphatics erosion (if the lesion erodes into a lymphatic) -lymph node and spleen involvement/ enters thoracic duct goes to heart and bloodstream
  5. Death
24
Q

explain what a scrofula is

A

Its a oropharyngeal TB with lymph node involvement. If you get TB in cervical lymph nodes then it erodes onto the skin its caled scrofuladerma

25
Give clinical features of primary TB and secondary TB
Primary TB: mostly asymptomatic | secondary TB: Fever, malaise, weight loss, night sweats, anorexia, chest pain, productive cough.
26
Give oral manifestations of TB
- Chronic, painless ulcer/nodular lesion - TB osteomyelitis of jaw (with military TB) - scrofula = oropharyngeal TB with lymph node involvement due to drinking infected milk, scrofuloderma- skin involvement. - Calcified cervical lymph nodes- ddx sialolith (seen on pan)
27
What special investigations are done for TB?
1. Biopsy- necrotising granulomatous inflammation | 2. Ziehl neelsen stain- highlights the acid fast bacilli
28
Diagnosis of TB give it.
2-4 weeks after exposure T cell hypersensitivity reaction upon re-exposure TB skin test- inject into skin. Reaction indicates previous exposure, not active disease. A negative skin test cannot rule out TB, often negative in immunocomp pts other ways to diagnose TB: sputum test with ziehl neelson stain and culture. DO chest x-ray shows ghon focus and complex. Culture takes 4 weeks. mycobacterial PCR.
29
How do you manage a TB patient?
Multiagent drug therapy! 2/ more active drugs for months to a year. Give isoniazid, rifampin, pyrazinamide. Ethambutol and streptomycin also be used. DOTS (directly observed treatment short- course)
30
Necrotising ulerative gingivitis (NUG) is what kind of infection?
bacterial infection of the gingiva
31
causative agents of NUG?
- fusobacterium nucleatum - prevotella intermedia - porphyromonas gingivalis - treponema denticola - selenomonas species.
32
Give the predisposing factors for NUG
- Psychological stress - immune supression - smoking - trauma - poor nutritional status - poor oral hygiene - inadequate sleep - recent illness
33
Pathogenesis of nug?
stressed state leads to release of corticosteroids- altering CD4 and CD 8 cells. Therefore decreased neutrophil chemotaxis and phagocyte response. Release of epinephrine (adrenelin) then get local ischaemia. Prostoglandins cause pain and acute phase proteins cause fever. There is vasodilation causing erythema and vascular permeability causing oedema.
34
Give the clinical features of NUG
- Any age (often young adults and mulnourished) - inflammation, oedema, haemorrhage of interdental papillae. - papillae are blunted, craterlike area of necrosis surfaced by grey pseudomembrane. - foul odour and extreme pain - spontaneous bleeding, necrotic debris - LAD, fever and malaise
35
Give the complications of NUG
- spread to alveolar bone= NUP - spread to adjacent soft tissue- Necrotising ulcerative mucositis/stomatitis. - spread to overlying skin- NOMA (cancrum oris)
36
Give the management of NUG
- Address any underlying predisposing factors. - bacterial removal leads to resolution. - debridement: scale and polish and curettage. - Give antibiotics: amoxicillin 500mg capsules (look at ofc notes on prescribing) and metronidazole 400mg - Chlorhexiine mouthwash, saline or hydrogen peroxide mouthwash - ohi and address other oral factors - Follow up this patient.
37
Define NOMA (cancrum oris)
Rapidly progressive polymicrobial bacterial infection caused by normal microflora in immune supressed.
38
What causes NOMA?
Fusobacterium necrophorum and prevotella intermedia
39
Give the predisposing factors of noma
``` Social factors malnutrition and dehydration poor OH illness/malignancy immune supression Begins as NUG ```
40
Give the clinical features and pathogenesis of NOMA
- NUG spreads to soft tissue then get mucositis/stomatitis with necrotic areas - necrosis spread to deeper soft tissues looks like blue black zone in skin over necrosis. - yellow zones of necrosis also over skin - spreads to bone get get osteomyelitis - foul smell, pain, fever.
41
Give the management of NOMA
- Always address the predisposing factors! - Antibiotics given (metronidazole and penecillin NB know a presciption) - conservative debridement! (for fungi infection do extensive aggressive debridement eg: mucormycosis!) - reconstruction after complete healing - Treat any nutitional problems, hydrate and elecrolyte imbalance
42
What is the prognosis of patients with NOMA?
Death due to pneumonia, septicaemia, facial disfigurement, local distubed growth. 10% die
43
Actinomycosis is what type of infection caused by what?
Bactterial infection caused by actinomyces species
44
Give the pathogenesis of actinomycosis
- Acute and rapidly progressive or chronic and fibrosing - 55% is cervico-facial - trauma- access for organisms to enter soft tissue - induces peripheral fibrosis - infect bone getting osteomyelitis
45
Give the clinical features of actinomycosis
- Yellow flecks- sulphur granules discharge from tissues - painless, tissue is hard and fibrotic - common site is angle of mandible!
46
How do we diagnose actinomycosis?
- biopsy and culture - culture takes long, and positive in 50% of cases only! - macrocopically can see the sulpur granules
47
How would one manage actinomycosis?
- Prolonged high dose antibiotics (penecillin/amoxicillin- tetracyclin if allergic). - Excision of sinus tract - Drainage of abscess - Debride necrotic tissue and bone - NB follow up with patient