Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

DTMH > Bacteria > Flashcards

Bacteria Flashcards

1
Q

Melioidosis - name of causative bacteria and bacteria description

A

Burkholderia Pseudomallei
Gram neg rod
Oxidase positive
environmental pathogen
multiple morphotypes
growth is always significant –> never a contaminant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Distribution of Melioidosis

A

Australia, SE asia, South america

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Methods of contraction of Melioidosis

A

soil + water contact
ingestion
subcut innoculation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Symptoms of melioidosis

A

Fever + pneumonia + abscesses
parotid abscess
spleen and liver abscess
lymphadenopathy
pneumonia
skin vesicles
brain abscess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Investigations and findings of melioidosis

A

CXR - patchy non-specific opacities
Micro - various patterns of growth
Sputum culture
Throat swab
Urine culture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Treatment of melioidosis

A

Ceftaz or meropenem - at least 2 weeks
then Bactrim for atleast 3 months

fevers can take weeks to improve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Anthrax - name of causative bacteria and its description

A

Bacillus Anthracis
gram positive
Spore forming bacteria
Anaerobic (but can be aerobic)
Non-motile
Non-haemolytic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Zoonosis animals for anthrax

A

Sheep
Cows

  • causes haemorrhage in animals (at higher infection levels)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Method of inoculation

A

Inhalation
Infected meat
IVDU
Skin (cutaneous anthrax)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Reason for anthrax virulence

A

Encapsulated
Has endotoxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Symptoms of anthrax

A

Oedema
Haemorrhage
Cutaneous anthrax - painless ulcer with eschar (can also occur in GIT and cause ulcers and peritonitis/perforation)
mediasteinal lymphadenopathy
pulmonary haemorrhage
Anthrax meningitis - bloody CSF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Treatment of anthrax

A

PEP
Vaccination
doxycycline or ciprofloxacin (add clinda if severe)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Plague bacteria and description

A

Yersinia Pestis
Gram neg
non-motile
Cocco bacilli - safety pin appearance
Aerobic non-lactose fermenter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Zoonotic host of plague

A

Rats - humans are an accidental host
Increasing incidence with deforestation and movement of forest rats into urban environments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Symptoms of plague

A

Fever
Pustules (Bubonic)
Pneumonia (Pneumonic)
Malaise
Shock
DIC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Investigation findings in plague

A

Neutrophillia
Lymphocytosis
Thrombocytopenia
DIC
Hepatorenal failure
Blue on Waysons stain (methelyene blue)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Treatment for plague

A

Streptomycin, Gentamicin, Bactrim, Ciprofloxacin, doxycycline
(gram neg cover)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the two types of rickettsial disease

A

Typhus group
Spotted fever group

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the Typhus group rickettsial diseases and their vectors

A

Epidemic - Louse
Marine (Endemic) - Flea
Scrub - Mite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the Spotted fever group rickettsial diseases and their vectors

A

Rocky spotted mountain fever
African tick fever
Mediterranean spotted fever
Rickettsial pox

All caused by ticks except rickettsial pox (mites)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Rickettsial bacteria description

A

obligate intracellular gram negative organisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Symptoms of rickettsial infection

A

Headache
Fever
Rash
Myalgia
Arthralgia
Eschar at bite sites
Pneumonia - ARDS
AKI

Rare - CNS disease, myocarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Rickettsia treatment

A

Doxycycline 7-10 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Q fever organism and description

A

Coxiella Burnetti
obligate intracellular coccobacillus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Hosts and vector for Q fever

A

Farm animals
Sylvatic animals
Vector –> Ticks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Issue with Q fever diagnosis

A

Can change its antigenic composition in lab conditions –> very difficult to grow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Q fever symptoms

A

Subclinical flu-like prodrome
Acute –> fever, hepatitis, atypical pneumonia.
Chronic –> endocarditis, arthritis, GBS, CNS.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Treatment for Q fever

A

Doxycycline 2-3 weeks (12 months if endocarditis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Name and description of bacteria causing trachoma

A

Chlamydia Trachomatis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Routes of trachoma transmission

A

4Fs

Food
Fomites/Fingers
Flies
Family

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Symptoms of trachoma

A

Repeated cycles of eye infection
red, watery, discharging eyes.
Causes eyelashes to grow inwards
Over time can have entropion from scarring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Stages of trachoma

A
  1. Normal
  2. Inflammation
  3. Intense inflammation
  4. Scarring
  5. Trichiasis (eyelashes inwards)
  6. Corneal opacification
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Types of spirochete infections

A
  1. Treponema- Pallidium (Syphillis),Yaws, Bejel, Pinta.
  2. Leptospirosis
  3. Borrelial disease - Relapsing epidemic borrelia (Louse borrelia), Relapsing endemic borrelia (Tick borrelia), Lyme disease.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Description of spirochetes

A

spiral structure, gram negative anaerobic rods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Diagnosis of spirochetes

A

Serology only - very difficult to culture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Epidemiology and transmission of Yaws

A

Is a disease in children
From skin-skin contact
increased in humid environments and around equator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Symptoms and stages of Yaws

A

Primary: Mother lesion at site of innoculation - can then develop satellite daughter lesions.
Secondary: Widely disseminated lesions via lymphatic spread, hyper keratotic. Affects palms and soles (causing crab walk)
Latent: symptoms resolve
Tertiary: Bone, joint and tissue involvement (classic nose disfigurement)

(think yams and crab)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Epidemiology and transmission of Bejel

A

In children
North Africa and middle east only
Skin-skin or mucous-mucous contact
Long latency - 3 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Treatment of Treponemal diseases

A

IM injection of Benzethine Penicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Symptoms and stages of Bejel

A

Primary: Painless chancre, common around nipples.
Secondary: Involvement of mucous membranes and genital lesions (condylomata lata), lymphadenopathy, osteoperiostitis.
Latent:
Tertiary: Destructive skin/bone gummas, skin depigmentation, neuro and cardiac involvement.

(bejewelled nipples and genitals)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Epidemiology and transmission of Pinta

A

Occurs in young adults in South America
Skin-skin contact
Most benign - skin ONLY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Symptoms and stages of Pinta

A

Primary: Plaque on arms/legs/hands - slowly enlarges
lymphadenopathy
Secondary: Disseminated lesions
Tertiary: Atrophic lesions and depigmentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Treponemal disease diagnostics

A

RPR/VDRL
Treponemal tests
PCR
Dark field microscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Borrelia types and vectors

A

Relapsing fever epidemic - louse
Relapsing fever endemic - soft tick (intended hosts are rodents and lizards)
Lyme disease - Hard tick

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Epidemiology of epidemic relapsing fever (borrelia)

A

high mortality associated with over-crowding and poor hygiene
Incubation - 1 week
More severe than tick borne borrelia - 70% mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Epidemiology of endemic (tick born) relapsing fever (borrelia)

A

found in the tropics
ticks live in roofs
passed down verically through tick generations
multiple relapses (10+)
10% mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Symptoms of borrelial disease

A

relapsing fevers lasting 3-6 days with each episode.
high grade fever, chills, myalgia.
Headache, confusion.
Hepatomegaly, jaundice.
Bleeding, petichiae
Myocarditis
DIC, thrombocytopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Diagnosis, management and complications of borrelial disease

A

Diagnosis - PCR
Management - Penicillin/Tetracycline

Complication - Jarisch - Herxheimer reaction (occurs in 2%) - exacerbation of fever and rash sometimes with hypotension, can also have other organ dysfunction.
Could be avoided with TNFa blockade (though not largely available)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Control measures for borrelia

A

Delousing
DDT, Permethrin, Malathion
Heat sterilisation of clothing
Mass PrEP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Lyme disease bacteria

A

Borrelia Burgdorferri

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Symptoms of Lyme disease

A

Erythema chronicum migrans (target like lesions)
Meningitis
Rediculopathy
Myocarditis
AV block

Late symptoms:
Arthritis/dermatitis/chronic fatigue
Encephalopathy/myelopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Treatment for Lyme disease

A

doxycycline 3 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Leptospirosis epidemiology

A

Is a zoonotic disease - many hosts and serotypes
Shed by animals through urine - contaminates soil and water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Phases of leptospirosis

A

Leptospiremic phase - blood and CNS
Leptospiuric phase - in urine and organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Symptoms of leptospirosis

A

Hepatitis/jaundice
Muscle necrosis
renal failure
Uveitis and subconjunctival haemorrhage
Aseptic meningitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is Weil syndrome

A

Complication of leptospirosis
End organ damage + haemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Treatment of leptospirosis

A

doxycycline (Penicillin if severe)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Brucellosis epidemiology and transmission

A

gram negative cocco-bacillus, commonly intracellular
found in Mediterranean and the Middle east
comes from animals (animals are well besides foetal loss)

Inhalation, dairy products (can be treated with pasteurisation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Symptoms of brucella

A

Undulating fever (rising and falling)
Anorexia, lethargy, fever, headache, lymphadenopathy
splenomegaly, hepatomegaly
Septic arthritis
Spinal disease
Orchitis
Hypersensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Brucella diagnostics

A

Culture - with Castaneda medium
Serology –> note can be paradoxically negative in high titres (due to lack of agglutination)
16S
Direct brucella PCR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Treatment of brucella

A

Doxycycline + second agent for 6-12 weeks

2nd agent - streptomycin, gentamicin, bactrim, rifampicin, fluroquinolones.

3 weeks doxy as PEP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Tuberculosis bacteria description

A

Weakly gram positive, Acid fast bacilli
Fungus-like
Very slow growing - generation time - 17hrs
Has a cell wall

63
Q

Immune evasion methods of TB

A

lives intracellularly (primarily in macrophages)
hides in vacuole to evade immune detection
Has immunomodulatory surface proteins

64
Q

Cause of TB granulomas

A

Caused by the body trying to wall off the infection.
less likely to see granulomas in immunocompromise (HIV)

65
Q

Life time risk of TB activation in latent persons

A

10%

66
Q

Latent TB tests

A

Tuberculin skin test - intradermal injection of TB antigens to see if there is immune reaction (delayed hypersensitivity reaction) - can have cross-reactivity with other types of mycobacterium. - Sensitivity 56%
Quant gold - ELISA based interferon gamma release assay - Sensitivity 78%
Elispot test - cytotoxic t-cells producing interferon gamma.

67
Q

TB diagnostic tests

A

Zeihl-Neelson stain
Fluorescent microscopy with auramine
Mycobacterial culture
Gene Xpert - NAAT
Gene Xpert ULTRA
CXR
Urine LAM - used in HIV+ cases

68
Q

Relationship between TB and HIV

A

HIV increases TB risk 20-40 fold
TB risk increases prior to CD4 count dropping - Early loss of pulmonary CD4 cells and altered innate responses of macrophages.

69
Q

Best timing of 3x AFB (sputum smear) collection

A

Spot/Spot/Morning

70
Q

Standard TB treat

A

HRZE (2 months) + HR(4 months)

71
Q

Standard TB treatment side effects

A

Rifampicin - orange secretions, liver injury, drug interactions, itch, flu-like symptoms,

Isoniazid - liver injury, peripheral neuropathy (give B6), psychosis

Pyrazinamide - arthralgia, gout, hepatotoxicity, GI upset, itch

Ethambutol - optic neuritis

72
Q

Treatment for CNS TB

A

HRZE 2 months + HR 10 months (12 months total)
Could consider adding steroids if HIV negative ONLY

73
Q

Issues with pleural TB diagnosis

A

pleural TB is considered extra-pulmonary (though often also have pulmonary disease)

AFB smear negative 98% of the time.
Poor sensitivity (around 50%) of culture and Gene Xpert

74
Q

effect of TB treatment on granulomas

A

Initial paradoxical enlargement - then improves

75
Q

Management of DILI from HRZE

A

Cease all drugs then re-introduce one by one slowly. Consider keeping off Pyrazinamide.

76
Q

CNS TB probability score

A

Marais score

77
Q

CSF findings in CNS TB

A

Appearance - slightly cloudy
Cell count - 100-500 (high but not as high as bacterial
High protein
Low glucose

78
Q

Group where TB diagnosis is commonly missed

A

Children <5

79
Q

What is gibbus deformity

A

bending of the spine due to spinal TB

80
Q

Paediatric TB symptoms

A

non-tender lymphadenopathy
Hard, painless abdominal swelling
Slowly arisen swollen joint
Wheeze not reactive to bronchodilators
Meningitis
Angular deformity of the spine

81
Q

Diagnosis of TB in paediatrics

A

Same methods as adults
Lower yield, more false negatives (smaller volumes of CSF etc)

Highly dependant on scoring systems –> CHILD TB LP and Keith Edward system

82
Q

Management of newborns in TB positive mothers

A

Give BCG at 3-6 months if baby has not contracted TB
Give isoniazid preventative therapy 10mg/kg for 6 months
If baby gets TB then treat with HRZE

83
Q

Breastfeeding advice for mothers with TB

A

Should breast feed UNLESS MDR

84
Q

Paediatric TB treatment durations

A

Pulmonary TB - 6 months
Non-severe TB - 4 months
CNS/miliary/spine/joint TB - 12months

85
Q

Categories of drug resistant TB

A

Rif resistant TB - RRTB
Multi drug resistant TB (rif + isoniazid) - MDRTB
Pre- XDRTB - (rif + isoniazid + fluroquinolone)
Extensively DRTB = XDRTB (rif + isoniazid + fluroquinolone + Grp A drug)

86
Q

Group A drugs in TB

A

Fluroquinolones (Moxiflox, levoflox)
Linezolid
Bedaquiline

87
Q

Regimen for Isoniazid resistant TB

A

HRZE + Levofloxacin

Once Isonazid resistance confirmed –> it can be dropped to RZE + Levofloxacin

88
Q

Regimen for RR-TB or MDR-TB

A

Short (all oral) (9 months), if uncomplicated TB with no previous second line exposure.

4-6 months: bedaquiline + levofloxacin + clofazimine + ethionamide (AABC) + high dose isoniazid + pyrazinamide + ethambutol (hHZE)
followed by
5 months: levofloxacin + clofazimine + pyrazinamide + ethambutol
(ABZE)

Bedaquiline use in this regimen is always for 6 months.

Long course (18 months) - AAA + BB

Bedaquiline (6m) + Linezolid + Levofloxacin + Clofazamine + Clycoserine

89
Q

Who should you screen for TB

A

High risk populations - HIV, malnutrition

Not household contacts - No change in health outcomes with household screening - likely due to the amount of TB caught outside the house.

90
Q

TB prevention options

A

BCG vaccine - only useful in children
Isoniazid prevention therapy - for at risk groups/children/household contacts - 6 or 9 months isoniazid, 4 months rif, 3 months combo.

91
Q

Social effects of TB in low-income settings

A

Catastrophic costs in 20% of households
- further poverty and its consequences
- malnutrition
- loss of work and education opportunities
- stigma

92
Q

Leprosy bacteria description

A

Obligate intracellular bacteria - lives within macrophages
Acid fast bacilli
Slow generation time (12.5 days)

93
Q

Leprosy epidemiology

A

Asia, South America, Nigeria
1-20 year latency
only 5% develop disease

94
Q

Leprosy transmission

A

Droplet
Close contact
skin-skin contact

95
Q

What parts of the body are most affected by leprosy

A

Cool areas where temp <33

96
Q

Classification of leprosy

A

Tuberculoid (TT) leprosy = paucibacillary form.
Asymmetric
1-2 lesions, sharply defined red patches or hypopigmented patch
<10 cm.
Sensory loss and hair loss over lesion
nerves are thickened and tender on palpation over lesion

Borderline tuberculoid (BT) leprosy.
More lesions (5-20) + larger in size.
Asymmetrical
Satellite lesions
Sensory loss and hair loss over lesion

Borderline borderline (BB) leprosy
Asymmetric
Multiple lesions of varying size, shape, and distribution
Skin-coloured or erythematous.
Swiss cheese lesions
Sensory loss and hair loss over lesion

Borderline lepromatous (BL) leprosy
Widespread bilaterally symmetrical lesions
Macules, papules, and nodules of variable size and shape
Sensation and hair growth remain normal within a lesion
Characteristic glove and stocking numbness
Widespread peripheral nerve involvement.

Lepromatous (LL) leprosy = multibacillary form
Early symptoms of nasal stuffiness, discharge, and bleeding
Swelling and thickening of limbs with subsequent ulceration
Symmetric widespread poorly defined hypopigmented and erythematous macules with normal sensation + nodules and plaques
Widespread peripheral nerve involvement.

Characteristic leonine facies with thickening of the forehead, loss of eyebrows and eyelashes (madarosis), distortion of the nose, and thickening of the earlobes
Involvement of other systems

97
Q

Systemic symptoms of lepromatous leprosy

A

Eyes — corneal anaesthesia, keratitis, corneal ulceration, uveitis, glaucoma, irreversible blindness
Testes — orchitis, testicular atrophy, sterility
Liver — hepatitis, hepatic amyloidosis
Kidneys — glomerulonephritis, renal amyloidosis
Bones — osteoporosis, resorption of digits.

98
Q

Immunological difference between tuberculous leprosy and lepromatous leprosy

A

Tuberculous - lower bacterial load, cell mediated response
Lepromatous - higher bacterial load, antibody response

99
Q

Which gene increases risk of active leprosy

A

NOD2 variant

100
Q

Symptoms of leprosy

A

Hypopigmented or erythematous skin patches
Thickened nerves with neuropathy and sensory loss
Sensory disturbance
Motor loss
Ophthalmic disease - weakening of eye nerves/muscles (Lagopthalmos) - eyes unable to close leading to Iritis.
Immunologic reactions - fatigue, malaise, fever, neuritis, arthritis, iritis, and nasopharyngeal symptoms.
Collapsed nose
Perforated nasal septum
Lucio phenomenon (necrotizing vasculitis)

101
Q

What are lepra reactions

A

Lepra reactions are immunologic reactions in leprosy that may be induced by treatment

Type 1 reaction ‘reversal reaction’ : Delayed hypersensitivity to M.leprae antigens and increase in cellular immunity.
- lesions become more red/ulcerated/indurated
- nerves become painful/paralysis
- occurs mostly in borderline disease

Type 2 ‘erythema nodosum leprosum’: Acute immune complex vasculitis
- eruption of AFB positive nodules
- swollen nodes, joints and eyes
- headache
- occurs mostly in lepromatous disease

102
Q

Treatment for each Lepra reaction type

A

Type 1 reaction ‘reversal reaction’ : Prednisolone + reduce rifampicin

Type 2 ‘erythema nodosum leprosum’: Pred + MTX + Thalidomide

103
Q

Diagnostics for Leprosy

A

Skin biopsy + AFB
PCR
Serology (not reliable)

104
Q

Treatment for Leprosy

A

Rifampicin triple therapy: Dapsone + Rifampicin (monthly) + Clofazimine

Paucibacillary → 6 months
Multibacillary → 12 months

Single lesion → Rifampicin + Ofloxacin + Minocycline

105
Q

Side effects of Leprosy drugs

A

Dapsone SE → Methaemaglobinemia. Dapsone hypersensitivity syndrome (10% mortality).
Clofazamine SE → photosensitivity, hyperpigmentation.
Haemolytic anaemia in G6DP. Agranulocytosis

106
Q

PEP for leprosy

A

Single dose Rifampicin

107
Q

Chlamydia - symptoms, testing, complications and treatment

A

Symptoms - clear discharge, cervical motion tenderness, rectal infection, pharyngeal infection, conjunctivitis.
Testing - gram stain
Complications - PID, ectopic, infertility, reactive arthritis
Treatment - 1 week doxy

108
Q

Gonorrhoea - symptoms, testing, complications and treatment

A

Symptoms - green discharge, urethral pain
Testing - Gram stain (GNC)
Complications - PID, prostatitis, skin lesions, tenosynovitis
Treatment - Ceft + Azithro STAT

109
Q

Trichmonas Vaginalis - symptoms, testing, complications and treatment

A

Symptoms - strawberry cervix, clear DC
Testing - microscopy, NAAT
Complications -
Treatment - Metronidazole

110
Q

Mycoplasma genitalium - symptoms, testing, complications and treatment

A

Symptoms - Majority asymptomatic, PID, cervicitis
Testing - NAAT
Complications -
Treatment - doxycycline then azithromycin if not improved

111
Q

Bacterial Vaginosis - symptoms, testing, complications and treatment

A

Symptoms - Grey thin discharge
Testing -
Complications -
Treatment - Metronidazole

112
Q

Empirical therapy for PID

A

IM Ceftriaxone stat + doxy 100mg BD + metronidazole 400mg BD

113
Q

Treatment of Syphilis

A

Benzathine Penicillin + Doxycycline
Can get an acute Jarisch-Herxheimer reaction with treatment
Prednisolone if neurosyphillis

114
Q

Tropical ulcer STIs - symptoms, testing, complications and treatment

A

Chancroid - painful + buboe + Phimosis
LGV (chlamydia subtype) - multiple ulcers, anorectal involvement, lymphatic obstruction.
Donovanosis - painless, granulomas

Diagnosis - NAAT

Treatment - Azithromycin

115
Q

Features and causes of small bowel diarrhoea

A

watery, low frequency large volumes.

causes: viruses, giardia, cholera, cryptosporidium

116
Q

Features and causes of large bowel diarrhoea

A

bloody, mucous, high frequency small volumes.

causes - campylobacter, shigella, salmonella, amoeba, schisto, strongyloidiasis

117
Q

Most common cause of diarrhoea in Africa in children <5

A

Shigella

118
Q

Shigella bacteria type, infectious dose and species

A

gram negative bacilli
10 bacteria required for infection
1 week incubation

Sonnei - most common in high income countries
Flexneri - most common in low income countries
Boydii
Dysenteriae - type 1 shiga toxin

119
Q

Treatment for Shigella

A

Ciprofloxacin, Azithromycin
Zinc!

Can be prevented with chlorination

120
Q

Shigella investigations

A

microscopy, culture, PCR (no serology)

121
Q

Entamoeba histolytica incubation, infectious dose and investigations

A

Incubation - 1 week
infectious dose - 1000 bacteria
Ix - microscopy, faecal antigen, serology

122
Q

cholera bacteria and infectious dose

A

gram negative bacilli
comma shaped
infectious dose - 100 million

123
Q

Incubation and symptoms of cholera

A

incubation - hours - 5 days
symptoms - severe watery diarrhoea, Rice water stools, bloating, vomiting, ileus, muscle cramps.
75% asymptomatic

124
Q

What is cholera sicca?

A

fluids pooling within the gut (third spacing) - severe dehydration without major vomiting or diarrhoea. Rapid deterioration.

125
Q

How does cholera cause disease

A

via cholera toxin - affects Nacl/K/HCO3 exchange
mediated by Tox R gene

126
Q

cholera investigations

A

Dark field microscopy - darting vibrios
Dipstick
Confirmation by culture

127
Q

Management of cholera

A
  • cholera vaccine - 2 types, toxin sub unit B vaccine and whole bacteria vaccine.
  • Azithromycin
  • glucose containing fluid replacement
128
Q

Cholera serotypes

A

01 - classical (more symptomatic), El Tor (more prevelant)
0139

129
Q

Types of enteric fever

A

Salmonella Typhi
Salmonella paratyphi

130
Q

Typhoidal salmonella presentation

A

usually bacteremic
10% mortality without treatment
relapse is common
step-wise fever
vomiting
diarrhoea OR constipation
cough
hepatosplenomegaly
Rose spots
CAN BE BRADYCARDIC

131
Q

Complications of typhoid

A

delirium
intestinal perforation
pneumonia
DIC
bone and joint infections
gallbladder cancer

132
Q

typhoid incubation and number of bacteria needed to cause infection

A

1-2 weeks
10 million

133
Q

Typhoid pathogenesis

A

Salmonella typhi and paratyphi can go through the gut wall silently via M-cells past peyers patches without causing diarrhoea/inflammation

Is an intracellular pathogen in macrophages and lymphnodes

→ after 1-2 weeks the bacterial load is so high that it spills out into the bloodstream causing fever and illness.

Can return to the GIT when expelled into the bowel from the gallbladder bile. Salmonella then re-interacts with the GIT peyers patches, which now recognise the pathogen and cause inflammation causing diarrhoea.

134
Q

Diagnostic tests for typhoid

A

Blood culture (54% sensitivity)
Faecal culture (25% sensitivity. Cannot differentiate chronic carriers)
Transaminitis (mild)
Widal test - agglutination of antibodies (high false negatives)
Rapid diagnostics tests

135
Q

Treatment of typhoid

A

Ciprofloxacin/Ceftriaxone, Azithromycin

In Pakistan - need meropenem due to drug resistance

136
Q

management of asymptomatic typhoid carriers

A

need a prolonged course of treatment - can readily pass infection to others (think typhoid mary)

137
Q

Vaccines for Typhoid

A

2 available
- TY21a
- Vi vaccine (for multi-resistant strains)

138
Q

Non-typhoidal salmonella species

A

Typhimurium
Enteritidis

139
Q

How does non-typhoidal salmonella differ from salmonella

A

Non-typhoidal salmonella can have non-human hosts
More commonly does not cause bacteraemia (except in HIV and in African variant!!)
low mortality
self limiting and does not require treatment

140
Q

Symptoms of non-typhoidal salmonella

A

Fever
Pneumonia
Diarrhoea
anaemia
hepatosplenomegaly

141
Q

what is the non-typhoidal salmonella African variant

A

A variant found across Africa (except South Africa which has global variant)
is invasive and causes bacteremia, without enteritis

142
Q

Common causes of meningitis

A

N.Meningitidis - globally, serogroups A, B, C, W and Y most commonly cause disease. (Men B vaccine - new)
Strep pneumo / Strep suis
H. influenzae

(SNH)

143
Q

proportion of people who have meningococcal rash

A

33%

144
Q

What are Kernig and Brudzinsky sign

A

Kernig - pain on passive extension of the knee with flexed hip
Brudinski - hips and knees flex when neck is flexed

145
Q

Treatment of meningococcal disease

A

Cefalosporin
Penicillin + Cefalosporin in >60
Vanc + Cefalosporin if risk of resistance
Chloramphenicol + Bactrim if immunocompromised

No significant improvement with steroids

146
Q

Management of meningococcal close contacts

A

Ciprofloxacin STAT

147
Q

Diptheria incubation, transmission and pathogenesis

A

Exo-toxin producing
A subunit and B subunit
Incubation 2-5 days
Droplet spread
Most common in children

147
Q

Diptheria incubation, transmission and pathogenesis

A

Exo-toxin producing
A subunit and B subunit
Incubation 2-5 days
Droplet spread
Most common in children

148
Q

Diptheria symptoms

A

Causes tonsillar plaque (dirty white membrane) and lymphadenopathy

149
Q

Diptheria investigations

A

ELEK test - to see if toxin producing
Black dots on agar
Toxin can be diagnosed by PCR

150
Q

Management of diptheria

A
  • anti toxin
  • ben pen + azithromycin
  • give immunisation
  • ecg monitoring for toxin induced heart block
151
Q

Tetanus management

A

Ben Pen/ Metronidazole
Anti-toxin

152
Q

Characteristics of Noma

A

Age 2-5
Occurs on face
Well demarcated perimeter
Odour
Short time frame
Comorbidity

DTMH (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions