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Bacteria - gram -ve Flashcards

1
Q

Risk factor/transmission for brucellosis?

A

Goat milk unpasteurised
Aerosols

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2
Q

What is the micro of brucellosis?

A

Gram negative coccobaccili - intracellular

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3
Q

What are the hosts for brucella?

A

melitensis - sheep and goats
abortus - cattle
suis - pigs

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4
Q

What is the clinical syndrome of brucellosis?

A

Undulant fevers
Moldy smell
Migratory arthralgia and myalgia
Leukopenia and deranged LFTs
Abdo sx
HSM
10% urogenital
Meningoencephalitis (maybe more common in HIV)
Cardiac manifestations - highest risk of death
Stillbirths
Ddx endocarditis, TB, VL, autoimmune dx, enteric fever, malaria

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5
Q

What is the epidemiology of brucellosis?

A

Mediterranean, Middle East, Central Asia and Central America, Africa

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6
Q

What is Pedro Pons signs?

A

preferential erosion of the anterosuperior corner of lumbar vertebrae in Brucellosis

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7
Q

What is the treatment for brucellosis?

A

The gold standard treatment for adults is daily intramuscular injections of streptomycin 1 g for 14 days and oral doxycycline 100 mg twice daily for 45 days (concurrently).

Another answer suggested gent and doxy

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8
Q

How do you prevent brucellosis?

A

Pasteurise milk
PPE to prevent aerosols
Vaccinate animals
Surveillance

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9
Q

How is brucellosis diagnosed?

A

Biopsy: non caseating granulomas
Bone marrow gold standard
PCR (cannot persist for months)
Multiplex for species
Lots of serology - many non-specific - need two (eg Rose Bengal)
Nb risk to lab staff!

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10
Q

What is PEP for brucellosis

A

Doxy + rif for 3 weeks / or co-trim

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11
Q

What is the transmission of bartonella henslae?

A

Cat scratch!

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12
Q

What is the micro of b.henslae?

A

gram negative facultative

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13
Q

What is the clinical syndrome of b.henslae?

A

Nodes
Fever
Cardiac - endoarditis
CNS
Bone involvement rarely

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14
Q

What is the diagnosis of b.henslae?

A

PCR
Biopsy of warthin-starry

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15
Q

What is the treatment of b.henslae?

A

Azithromycin

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16
Q

What is the micro of leptospirosis?

A

Gram negative aerobic spirochete

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17
Q

What is the epidemiology of leptospirosis?

A

Occurs in rainy seasons

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18
Q

What is the host for leptospirosis?

A

Rats but also livestock, domestic animals, bats, marsupials

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19
Q

What is the clinical syndrome of leptospirosis?

A

Incubation around 7 days
Early phase: fever, myalgia, headache
Late phase: jaundice, renal failure, pulmonary haemorrhage

Uveitis, aseptic meningitis, myocarditis

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20
Q

How is leptospirosis diagnosed?

A

ELISA for IgM
PCR
DFM/MAT

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21
Q

How is lepto treated?

A

For treatment usually use oral doxycycline for mild cases – Doxycycline (100mg PO bid) or
– Amoxicilin (500mg PO tid) or Ampicilin (500mg PO tid)
SEVERE: intravenous penicillin and ceftriaxone for moderate to severe cases but…limited evidence
– Penilicin (1.5m units IV or IM q6h) or
– Ceftriaxon (2g/d IV) or Cefotaxime (1g IV q6h) or
– Doxycycline (loading dose of 200mg IV then 100mg IV q12h)

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22
Q

What is the micro of the plague?

A

Gram negative short pleomorphic cocco-bacillus
Non-sporing, non motile, Capsule
Bipolar staining

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23
Q

What is the vector + host for plague?

A

Parasite of rodents – tolerate chronic bacteraemia

Transmitted by flea bites (Oriental rat flea:
Xenopsylla cheopsis.
(80 flea species implicated)) on skin or ingestion of infected animal material (eating infected guinea pigs in Peru and camels in Asia!).

Sylvatic plague
Outbreaks of plague in susceptible animals
Ground squirrels, gerbils and voles
Bandicoots, marmots, squirrels, chipmunks, prairie dogs and rats Fleas transmit to man
Farmers or trappers

Urban plague
Spread among rats
Black rat Rattus rattus – common around human habitation Less transmission with brown (sewer) rat Rattus norvegicus Epidemic and pandemic

Pneumonic - human to human transmission

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24
Q

What is the clinical syndrome of PNEUMONIC plague?

A

1-3 days incubation period
Rapidly progressive pneumonia
Tachypnoea, dyspnoea, chest pain, cough, haemoptysis
Chest X-ray findings of primary or secondary pneumonia
Initial patchy segmental or lobar pneumonia Rapidly progression within hours or days Bilateral pulmonary consolidation, necrosis and haemorrhage
Contagious to close contacts by respiratory droplet spread Respiratory droplet precautions (universal/mask/eye protection)
[Negative pressure isolation not necessary]
Contact tracing, surveillance and chemoprophylaxis [7 days]

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25
Q

What is the epidemiology of plague?

A

Sporadic outbreaks
Only 6 countries in 2019-22 1722 cases – 175 deaths

MADAGASCAR!!

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26
Q

What is the clinical syndrome of BUBONIC PLAGUE

A

Bubonic (not contagious)
Incubation period of 2-7 days following bite
Sudden onset
Headaches, fever, malaise
Bubo – very painful, tender, erythematous swollen regional lymph nodes
Inguinal (most common), axillary, cervical
Infected skin lesion rarely detected
The majority of infective flea bites occur on lower limbs
May disseminate in blood to lungs and brain
Not contagious Chemoprophylaxis (household)

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27
Q

What is the diagnosis of plague?

A

WBC elevated with neutrophil predominance Platelet levels low
Liver and renal function may be deranged
Gram or Wayson stain of bubo aspirate or sputum Moderately sensitive and specific; Rapid
Culture of bubo aspirate, blood or sputum
Sensitive if patent untreated; specific; takes 2-3 days
Immunofluorescent antibody to aspirate or sputum Moderately sensitive, highly specific, rapid
Dipstick for F1 antigen in bubo aspirate Sensitive, specific and rapid
PCR for F1 gene in bubo aspirate Moderately sensitive, highly specific, rapid

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28
Q

What is the treatment for plague?

A

Streptomycin im 30mg/kg 2 doses daily 10days. (1948)
But: limited availability, side effects-renal, hearing.
Discontinued now except in Madagascar in combination with co-trimoxazole Gentamicin + doxycycline (Boulanger et al. CID 2004:38) (Tanzania, CID 2006:42) Ciprofloxacin (Other fluoroquinolones)
[Chloramphenicol – effective but rarely used - meningitis]
Fluoroquinolones, doxycycline, tetracycline, co-trimoxazole used as prophylaxis to prevent pneumonia
Cephalosporins – not recommended.

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29
Q

What is the prognosis of plague?

A

40-60% bubonic
100% pneumonic or septicaemic

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30
Q

What is IPC for plague?

A

Avoid fleas
Rodent control
PPE
funeral practice
PEP
Vaccine used by military
Surveillance for outbreaks

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31
Q

What is the micro of melioid?

A

Burkholderia pseudomallei
Gram negative bacilli

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32
Q

What is the epidemiology of melioid?

A

Case numbers – 165,000 annually

Deaths – 89,000 annually

Thailand – 3000-5000 cases yearly

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33
Q

What is the transmission of melioid?

A

Acquired through contact with contaminated water or soil through skin abrasions or aerosol (Seasonal)
Rice farmers in Thailand
Indigenous population in Australia
War wounds
Inhalation (helicopter pilots)
Ingestion of water (near-drowning, potable water) Laboratory-acquired
Person-person, animal-person very rare

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34
Q

What is the clinical syndrome of melioid?

A

Incubation: 1-29 d up to 29 y

Fever and rigors; lung and skin involvement; septic shock (20%) Jaundice, diarrhoea, reduced conscious level
Anaemia, neutrophilia, coagulopathy
Metastatic abscesses:
lungs (80% abnormal CXR, multifocal pneumonia, cavitations) liver, spleen, kidneys
skin and soft tissues; muscle and prostate
bones and joints; kidneys; brain
PAROTITIS

Untreated mortality 100%; 10-50% depending on level of care available

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35
Q

What is the diagnosis of melioid?

A
  • Biosafety level 3*
    Isolation
    Blood, urine, throat - sputum, pus,
    Unevenly stained Gram-negative bacilli
    Isolation from non-sterile sites increased by use of selective media (Ashdown’s, selective broth, 420C incubation)

Metallic sheen, sweet earthy smell

Serology - > 1:320 probable

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36
Q

What is the treatment of melioid?

A

Meropenem!
Drain abscesses
Supportive

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37
Q

What is the IPC of melioid?

A

No vaccine
Avoid contact - shoes in rice fields/diabetics

PEP for lab

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38
Q

What is the micro of salmonella typhi/typhoid?

A

Gram negative bacilli

Salmonella Typhi and Salmonella Paratyphi A

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39
Q

What is the epidemiology of typhoid fever?

A

10-20 m
100-200K deaths
++Asia India, Africa, S America

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40
Q

What is the clinical syndrome of typhoid?

A

Prolonged febrile illness with bacteraemia

Week 1 - fever, headache, abdominal pain, vomiting, cough

Week 2 - high grade fever, ++abdo, HSM, rose spots

Week 3 complications - GI bleed, perf, pneumonia

Week 4 - advanced illness, apathetic illness, agitated delirium

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41
Q

What is the diagnosis of typhoid?

A

Blood cultures (poor sens)
Widal test (agglutinating antibodies against O + H antigens) - high false neg rate, can cross react with other febrile illness
RDT

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42
Q

What are the complications of typhoid?

A

Gastrointestinal bleeding Perforation Encephalopathy/shock
Hepatitis Pneumonia Psychiatric
Relapse
Chronic carriage (> 1year)
Carcinoma of gall bladder
Meningitis
Myocarditis
DIC
Cholecystitis
Anaemia
Bone and joint

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43
Q

What is the treatment of typhoid?

A

Ceftriaxone/ cipro/SCA
nb lots of ceft resistance in Pakistan

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44
Q

What is the transmission of typhoid?

A

Faecal-oral transmission Water
Food
Hot season or flooding conditions

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45
Q

How long does defervescence take in typhoid?

A

3+ days

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46
Q

What is the prognosis of typhoid?

A

Relapse
Chronic carriage (> 1year) Carcinoma of gall bladder

90% uncomplicated
10% severe complicated disease
10% + mortality with no treatment
< 1% mortality if adequate treatment

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47
Q

How is chronic typhoid diagnosed and managed?

A

3 x faecal cultures
Vi antibodies
1-3 months abx

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48
Q

What is the vaccinology of typhoid?

A

Oral attenuated and polysaccharides available
Conjugated Vi much more effective than PS

New Vi WHO approved
No paratyphoid available

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49
Q

What are these?

A

Rose spots
Appear in typhoid

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50
Q

What is the micro of non-typhoidal salmonella (NTS)?

A

Gram neg bacilli

Typhiumrium
Enteritidis
> 2500 other Salmonella serovars

NOT paratyphoid

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51
Q

what is the epidemiology of NTS?

A

NTS 94 million cases (95% CI 62-132) 155,000 deaths (95% CI 39,000-303,000) 80 million cases foodborne

INTS 3.4 million (range 2.1–6.5) million
681,316 (range 415,164–1,301,520) deaths

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52
Q

What is the transmission of NTS?

A

Normal habitat of many serotypes is the gut of animals. Found in the food chain.
Ingestion of contaminated food or person to person.
Most infection foodborne
Meat, eggs and processed food (chocolate, peanut butter etc)
Chronic carriage possible (gut not gallbladder)

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53
Q

What is the clinical syndrome of NTS?

A

Diarrhoea (gastroenteritis)
Some cause invasive disease with bacteraemia (iNTS)
May lead to focal infection
Bones and joints Endovascular infection Meningitis (very young)
Extremes of life (very young, elderly)
Immunocompromised (malignancy, steroids, immunotherapy agents, DM, Sickle cell disease, HIV - AIDs defining if BSI)

In Africa: Often present as fever without localising signs Overlaps with malaria

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54
Q

What is the treatment of NTS?

A

Ceftriaxone
?2nd ppx until CD4 improves?
Start ART

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55
Q

What is the IPC of NTS?

A

Food hygiene
Manage HIV!
No vaccine

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56
Q

What makes INTS more prevalent in Africa?

A

In HIV -
Gut mucosal defect
Early and profound gut mucosal CD4 depletion (particularly Th17 cells)
More persistance
Impaired serum killing of NTS in HIV infected adults
IgG antibodies compete with bactericidal antibodies

Malaria
Macrophage dysfunction
Dysregulated cytokines

Sickle cell disease Homozygous at risk

Ineffective serum killing of NTS
Deficiency of anti-Salmonella IgG antibodies

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57
Q

what is relapsing fever?

A

Relapsing fever is an illness characterized by one or more episodes of fever, headache, and muscle pain that lasts several days and is separated by roughly a week of feeling well. Relapsing fever is caused by several species of Borrelia bacteria, which are distantly related to the bacteria that cause Lyme disease.

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58
Q

What are the two types of relapsing fever?

A

Tick and louse borne
Louse borne often more severe

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59
Q

How is relapsing fever treated?

A

1-2 weeks of a tetracycline

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60
Q

What causes Oroya fever?

A

Bartonella bacilliformis, transmitted by sandfly in south america

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61
Q

What is the clinical syndrome of Oroya fever?

A

Fever, severe haemolytic anaemia, jaundice, heart failure, effusions 3-8 weeks after bite

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62
Q

What is verruca peruana?

A

Bartonella baciliformis - after Oroya fever, developing angioproliferative lesions

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63
Q

How is Oroya fever treated?

A

Cipro plus Ceftriaxone if severe

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64
Q

What is the clinical syndrome of rickettsial infections

A
  • Incubation period: 5-14 days
  • Systemic endothelial infection resulting in lymphohistiocytic vasculitis
  • Non-specific febrile illness, relative bradycardia
  • Symptoms: fever, rash, eschar, headache, lymphadenopathy, malaise, myalgia, nausea,
    cough
    Severe disease: interstitial pneumonitis, interstitial nephritis, interstitial myocarditis,
    meningoencephalitis
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65
Q

What is the microbiology of rickettsia?

A

Obligate intracellular gram negative bacteria

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66
Q

Eschar in Asia might mean?

A

Scrub typhus

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67
Q

what is the cause of scrub typhus?

A

Orientia tsutsugamushi - million cases per year

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68
Q

What is the vector of scrub typhus?

A
  • Leptotrombidium
  • Only larvae (chigger) can transmit the disease
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69
Q

What is an eschar?

A
  • A necrotic lesion of the skin at the site of arthropod inoculation
  • No pain, no itchiness
  • An excellent sample for PCR testing
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70
Q

What causes Japanese spotted fever?

A
  • Rickettsia japonica
  • Vector: hard ticks (Dermacentor, Haemaphysalis)
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71
Q

What causes Rocky Mountain Spotted Fever (bacteria and vector)?

A
  • Rickettsia rickettsii
  • Vector: Dermacenter ticks, Rhipicephalus ticks, Amblyomma ticks
  • ‘Wait for a host in an ambush strategy falling onto a hairy host from a height of 1 m’
  • Frequently bite in the hair and targets children
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72
Q

Where does Rocky Mountain Spotted Fever occur?

A

Southern US and S America

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73
Q

What causes African tick bite fever (bacteria and vector)?

A
  • Rickettsia africae
  • Vector: Amblyomma ticks
  • Aggressive hunting ticks
  • Frequently attack in groups
  • Non host-specific (humans, cattle, wild ungulates)
    presents with MULTIPLE eschars occurs in outbreaks and clusters
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74
Q

Which rickettsia has multiple eschars?

A

African Tick Bite Fever

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75
Q

What causes Mediterranean Spotted Fever (bacteria and vector)?

A
  • Rickettsia conorii
  • Vector: Rhipicephalus ticks (dog tick)
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76
Q

What causes epidemic typhus (bacteria and vector)?

A
  • Rickettsia prowazekii
  • Vector: body louse (Pediculus humanus corporis)
  • Reservoir: human/flying squirrel
  • Transmission through close physical contact
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77
Q

Who gets epidemic typhus?

A
  • Prison, homeless shelter
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78
Q

What is the mortality of epidemic typhus?

A

Variable mortality up to 60%

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79
Q

What is Brill-Zinsser disease?

A

Epidemic typhus reactivation years after primary infection

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80
Q

What causes eNdemic typhus (bacteria and typhus)?

A
  • Rickettsia typhi/murine typhus
  • Vector: rat flea (Xenopsylla cheopsis), cat flea (Ctenocephalides felis)
81
Q

How are rickettsia diagnosed?

A

Clinical

Lab:
- PCR: eschar, skin rash biopsy, whole blood
- LAMP
- Bacterial culture: only available in limited reference laboratories
- Antibody - IFA (indirect immunofluorescent assay) considered gold-standard

82
Q

What is diagnostic of antibody titres in rickettsial illness?

A

Four-fold titre increase in paired samples

83
Q

Name three agglutination tests?

A

Widal test for typhoid fever, MAT for leptospirosis, SAT for brucellosis

84
Q

How are rickettsia treated?

A
  • Doxycycline
  • Inhibition of protein synthesis
  • Excellent penetration to the intracellular space
  • Azithromycin, chloramphenicol * β-lactams are not effective
  • Inhibition of cell wall (peptidoglycan) synthesis
  • Poor penetration to the intracellular space
  • Defervescence within 48 hours
85
Q

What is the IPC of rickettsial infections?

A

Administrative control
* Raise awareness among patients and healthcare workers
* Improve sanitation (epidemic typhus)
* Vaccine development (no vaccine so far…)
Environmental control
* Clean bushes and weeds
* Cut grass close to the ground
* Prevent rat infestation
Personal protection
* Avoid tick/mite bite (repellent, protective clothing)
* Careful inspection for ticks/mites after outdoor activity
* Wash clothes (epidemic typhus)
* DOXY prophylaxis is not routinely recommended

86
Q

What kind of pathogen is rickettsia group?

A

Bacteria
Gram negative
Bacilli
Intracellular

87
Q

What is the clinical syndrome of rickettsial infection?

A

Fever + rash + eschar

Incubation = 5-14 days

88
Q

What do routine bloods demonstrate in rickettsial infection?

A

Low WCC, atypical lymphocytes, eosinophils 0

Low platelets

High CRP, high LFT

89
Q

Scrub typhus causative organism

A

Oriensia tsutsugumashi

90
Q

What are the three groups of rickettsial infection?

A

Scrub
Spotted fever
Typhus

91
Q

Vector of scrub typhus?

A

Mite - larval stage
Trombeculae (“chigger”)

92
Q

Reservoir of scrub typhus?

A

Rat, other rodents

93
Q

Distribution of scrub typhus?

A

Disease of rural area

Asia, Pacific, Northern Australia

94
Q

Clinical syndrome of scrub typhus?

A

Fever + rash + eschar
Incubation: 5-14 days

Rash: maculopapular. Trunk -> extremeties, palmar sparing

Associations: faget’s, pneumonitis, deafness, lymphadenopathy, HSM, myocarditis, delirium

95
Q

Vector + reservoir for spotted fever group rickettsia?

A

Vector = hard ticks

Reservoir = dogs, rats, cattle

96
Q

Japanese spotted fever causative organism and vector?

A

Rickettsia Japonicum
Hard tick (dermacentor, haemaphysalis)

97
Q

Japanese spotted fever clinical syndrome

A

Fever + rash + eschar
Incubation: 2-8 days
Rash: extends to palms and soles

Associated with severe disease

(Shorter incubation and palmar rash distinguishes from scrub typhus)

98
Q

Rocky Mountain spotted fever causative organism and vector

A

Rickettsia rickettsii
Hard tick: dermacentor (ambush type)

99
Q

Rocky Mountain spotted fever clinical syndrome

A

Fever + rash, eschar absent
Incubation 3-12 days
Rash 2 days after fever onset

Severe disease, fatality ~10%, highest in children

100
Q

African tick bite fever causative organism and vector

A

Rickettsia Africae
Ambyloma tick (ambush type)

101
Q

African tick bite fever clinical syndrome

A

Spotted fever group

Fever + multiple eschar (aggressive tick) + regional lymphadenopathy, rash rare

Incubation = 5-10 days

Mild disease

102
Q

Epidemic typhus causative organism and vector

A

Rickettsia Prowazeki
Human body louse

103
Q

Epidemic typhus clinical syndrome

A

Typhus sub group

Fever + maculopapular rash, no eschar (infected faeces –> bite site)

Incubation 10-14 days

Seen in areas of close contact and poor sanitation, eg prisons, shelters

Severe disease –> pneumonia, meningoencephalitis, myocarditis, death

104
Q

What is Brill-Zinner disease?

A

Recrudescence of epidemic typhus in partially treated, occurring years later

105
Q

Endemic (/murine) typhus causative organism and vector

A

Rickettsia typhi
Rat / cat flea

Reservoir = rat, cat (unsurprisingly) + opossum (cute xx)

106
Q

Endemic typhus clinical syndrome

A

Fever + rash + headache + no eschar (infection via infected poo –> itched into bite site)

Incubation 7-14 days

Occuring worldwide, anywhere with rats

Mild disease

107
Q

How are rickettsial infections diagnosed?

A

Usually clinical: fever + rash + eschar

Gold standard = IFA (indirect immunoflourescence assay) - not positive until ~7/7 of illness as antibodies not yet established

PCR of blood / eschar / rash biopsy

Culture of organism difficult

Serology (Weil Felix) for direct / indirect agglutination tests (antibody : antigen)

Lots of x reaction in serological tests between spotted fever groups and also with syphilis

108
Q

How do you treat rickettsial infection?

A

Doxy for all :))
- Duration based on subtype, aim 7-10/7
- IV if severe

Pregnant women, children:
- doxy if severe
- azithro if mild

Defervescence within 48 hours

109
Q

How do you prevent rickettsial infection?

A

ENVIRONMENTAL:
- Clear bush and scrub, keep grass short
- Keep rats away
- Improve sanitation (esp epidemic typhus as lice borne)

PERSONAL:
- Prevent bites (repellent, long clothing)
- Education: keep away from high risk areas eg bush walking, check carefully for bites on return
- Hygiene: wash clothing and bedding well (esp epidemic typhus as lice borne)

No vaccine
Routine doxy prophylaxis not recommended

110
Q

What causes Lyme disease?

A

Borrelia burgdorferi
Gram negative spirochete

111
Q

What is the vector for Lyme?

A

Ixodes ticks

112
Q

What is the epidemiology of Lyme disease?

A

200k pa
Temperate regions

113
Q

What is the clinical syndrome of Lyme disease?

A

Erythema migraines - target lesion/central clearing. At this point, 50% seronegative

Early disseminated: arthralgia
Neuro (15% seronegative - > need LP)
- Radicular pain
- Cranial nerve palsies
- Peripheral paresis
- Headache
- Intermittent fever
- Rarely, encephalitis

Late disseminated:
Large joint arthritis
Encephalitis

114
Q

How is Neuroborreliosis diagnosed?

A

Early can be clinical -> typical rash and history of tick bite

Serology: lots of false pos. In 1st month - > IgM and IgG, after 1st month just IgG should be tested

For neuro
- Compatible symptoms
- CSF pleocytosis
- Positive intrathecal Borrelia antibody index test
Sens + spec 94-96%

115
Q

How is Lyme treated?

A

Usually doxy. Treatment regimens for Lyme disease range from 14 days in early localized disease, to 14–21 days in early disseminated disease to 14–28 days in late disseminated disease

Neuro: 14 days doxycycline, ceftriaxone or benzylpenicillin

116
Q

What is the IPC of Lyme?

A

Dress appropriately
Repellants
Watch for ticks
Deer control in US
No vaccine yet

117
Q

what is the microbiology of tularaemia?

A

Francisella tularensis
Gram negative coccobacilli

118
Q

What is the epidemiology of tularaemia?

A

Tularemia is most common in the Northern Hemisphere, including North America and parts of Europe and Asia.[24] It occurs between 30° and 71° north latitude

119
Q

What is the host and vector of tularaemia?

A

Biting flies and ticks include Amblyomma and Ixodes Rodents, rabbits, and hares often serve as reservoir hosts = RABBIT FEVER!!

120
Q

What is the transmission of tularaemia?

A

Contacted with infected animals
Vector borne
Aerosolised (lawnmow a fucking rabbit!)
Lab
Contaminated water
Bioterrorism

121
Q

What is the diagnosis of tularaemia?

A

Special media such as buffered charcoal yeast extract agar.

Serological tests - cross reactivity with Brucella can confuse interpretation of the results

PCR in ref labs

122
Q

What is the clinical syndrome of tularaemia?

A

tularemia has six characteristic clinical variants: ulceroglandular (the most common type representing 75% of all forms), glandular, oropharyngeal, pneumonic, oculoglandular, and typhoidal

Can look a bit like the plag

123
Q

What is the treatment of tularaemia?

A

Gentamicin, long doxy or fluoroquinolone

PEP for lab is doxy

124
Q

what is the IPC of tularaemia?

A

Prevention is by using insect repellent, wearing long pants, rapidly removing ticks, and not disturbing dead animals.

125
Q

What are the important typhoid/typhus?

A

Salmonella typhi/paratyphi -> typhoid fever

Rickettsia typhi -> Murine typhus (endemic typhus)

Rickettsia prowasekii -> Typhus (epidemic typhus)

Orientia tsutsugamushi - > scrub typhus

126
Q

What is the causative agent for Q fever?

A

Coxiella burnetii
Gram neg intracellular

127
Q

What is the transmission of Q fever?

A

Cattle, sheep, goats, can be tick borne

128
Q

What is the clinical syndrome of Q fever?

A

Acute: pneumonia/hepatitis
Chronic:Almost exactly like endocarditis
Small proportion very sick

129
Q

What is the epidemiology of Q fever?

A

Global

130
Q

What is the diagnosis of Q fever?

A

Serology
Blood cultures rubbish
PCR possible but low sens after acute
APLS abx pos in those with chronic
TOE
CT-PET

131
Q

What is the treatment of Q fever?

A

Doxy pls HCQ to prevent APLS type issues

14d acute
18-24 MONTHS if chronic
HCQ until no APLS abx

132
Q

What is the IPC of Q fever?

A

Avoid unpasteurised milk
Avoid animals
Vaccine in Australia

133
Q

Leptospirosis causative organism

A

Leptospira species (>200)
Spirochete
Weakly staining gram negative

134
Q

How is leptospirosis contracted

A

Water contaminated with infected rat / livestock urine and faeces comes into contact with broken skin / mucosa

Human : human transmission not seen

135
Q

Who gets leptospirosis?

A

People after flooding

Sewage workers

Farmers

Recreational water sports in gross water like canals

136
Q

Lepto incubation

A

10 days

137
Q

3 clinical syndromes of lepto

A
  1. asymptomatic
  2. self limiting (sudden onset fever + myalgia of calves and back + conjunctival injection)
  3. severe / weils: fever + jaundice + haemoptysis + resp and renal failure

Fatality 20% in jaundiced, 2% in others

138
Q

How is leptospirosis diagnosed?

A

MAT (microscopic agglutination test)

PCR urine / serum

Culture slow and insensitive, serology unreliable

139
Q

How is leptospirosis managed?

A

Mild: doxycycline

Moderate / severe: benpen

Beware Jarisch - Herxheimer: high fever + shock after abx in spirochetal infection. Manage supportively, continue abx.

140
Q

How can leptospirosis be prevented?

A

PPE for sewage / farmers (gloves, boots)

Reduce exposure (no swimming in the canal)

Control rodents

Vaccinate livestock (no human vaccine)

Prophylactic weekly doxycycline (reduces severity but not infection itself)

141
Q

Melioidosis causative organism

A

Burkholdelia Pseudomallei
Gram -ve rod
Bipolar staining (safety pin)

Lives in surface water on rice paddies

142
Q

Melioidosis distribution

A

Thailand
SE Asia
Caribbean

Anywhere with surface water, esp rice paddies

143
Q

How is melioidosis transmitted?

A

Not human to human

Ingestion / inhalation / inoculation of burkholdelia pseudomallei

144
Q

Melioidosis clinical syndrome plus incubation

A

Incubation 1 day - 60 years, usually acute

Acute sepsis: pneumonia, liver / splenic abscess / parotitis / prostatitis / pretty much any organ system

Chronic: fever, weightloss, wasting. Latent disease recurs even after 30 years

145
Q

How is melioidosis diagnosed?

A

Culture of any sample (blood, urine, pus, throat swab)
BEWARE: biohazard level 3, please think of Calvin and warn the lab staff

146
Q

How is melioidosis managed?

A

3/12 abx total. 9 days to defervesce

10/7 IV = ceftazidime / meropenem

3/12 PO to clear infection = trimethoprim sulfamethoxazole

10% recurrence if not cleared effectively

Image for deep seated infection, drain where possible

147
Q

What is the fatality rate of melioidosis?

A

40%
Rapid fulminant sepsis usually

148
Q

What is the causative organism of cat scratch disease

A

Bartonella Henselae

Gram negative intracellular bacillus

149
Q

What is the clinical syndrome of cat scratch disease

A

Painful local lymphadenopathy around the scratch / bite, self limiting 3/12

Rare complications = retinitis, encephalopathy, endocarditis, bartonella angiomatosis

150
Q

How is cat scratch disease spread

A

Bite / scratch from infected cat

Cat : cat via flea

151
Q

How is cat scratch disease diagnosed

A

Serology (x react with bartonella quintana)

PCR blood / wound

Histology Warthin - Silver Starry stain –> angiomatosis lesions

Culture impractical

152
Q

How is cat scratch disease managed

A

Usually self limiting

Short course azithromycin, longer if bartonella angiomatosis present (2 months)

153
Q

What is the causative organism of trench fever

A

Bartonella quintana

Gram negative intracellular bacillus

154
Q

What is the transmission of trench fever

A

Human body lice (pediculus humanis)

Poor living conditions

155
Q

What is the clinical syndrome of trench fever

A

Short incubation, rapid onset

High fever + retro-orbital pain + bone pain usually shins

May follow relapsing remitting pattern

Complications in immunocompromised:
Culture negative endocarditis, bacillary angiomatosis

156
Q

How is trench fever diagnosed?

A

Serology (x reaction with bartonella henselae)

PCR

Culture impractical

157
Q

How is trench fever managed?

A

Doxycycline 4/52 plus gentamcin 2/52

Endocarditis= ceftriaxone + gent

158
Q

What is causative organism of Carrions / Oroya / Verruga Peruana?

A

Bartonella bacilliformis

Gram negative intracellular bacillus

159
Q

What is clinical syndrome of Oroya fever

A

Children / travelers to Peruvian Andes
Long incubation, ~2 months

Sepsis + haemolysis

Multiple organ failure + death not uncommon

160
Q

What is clinical syndrome of Verruga Peruana

A

Multiple nodular / papular skin lesions, tender

Adults in Peruvian Andes

+/- history Oroya fever

161
Q

How is Oroya fever / Verruga Peruana diagnosed?

A

Serology / PCR
Histology of skin lesions

Culture (biosafety level 3)

162
Q

How is Oroya fever managed?

A

Ciprofloxacin 10/7

163
Q

How is Verruga Peruana managed?

A

Rifampicin / streptomycin reduces number and pain of skin nodules but usually self limiting

164
Q

How is Oroya Fever / Verruga Peruana transmitted?

A

Infected sandfly bite (lutzomyia)

Rats and domestic animals = reservoir

165
Q

Brucellosis causative organism(s)

A

Gram -ve coccobacilli

B. melitensis most common
(camels, goats, sheep)

B. Abortus (camels, cows)

B. Suis (pigs)

B. Canis (dogs)

166
Q

How is brucella transmitted? (4 ways)

A
  1. Ingestion unpasteurised dairy from infected animal
  2. Direct contact with body fluid of infected animal
  3. Infected blood transfusion
  4. Human breast milk
167
Q

What is clinical syndrome of brucellosis?

A

Long incubation (weeks - months), subacute presentation. Faget’s

Fever + lymphadenopathy + HSM + constitutional symptoms + localising sign of complications

BONE –> arthritis, sacroilitis

REPRODUCTIVE –> spontaneous abortion, epididymoorchitis

CNS –> abscess, meningoencephalitis

ENDOCARDITIS –> most fatal

168
Q

How is brucellosis diagnosed?

A

Routine: Low WCC, Low Plt, Deranged LFT

RDT
Serum agglutination (x reactivity)
Serology (IgM IgG IgA)
Culture slow, dangerous for lab staff. Bone marrow most sensitive

169
Q

How is brucellosis managed?

A

Long course abx needed to prevent recurrence. 6/52

Doxy + rifampicin + gent / streptomycin

170
Q

How can brucellosis be prevented?

A
  1. Boil / pasteurise dairy
  2. PPE for at risk workers (vets, farmers, abbatoir)
  3. Vaccinate animals in outbreaks
  4. Correct handling of animal fluids and carcasses
171
Q

Plague causative organism

A

Yersinia pestis

Gram negative coccobacilli
Bipolar staining –> ‘safety pin’ appearance

172
Q

Plague global distribution

A

Madagascar
USA
DRC
Uganda
Tanzania

173
Q

Plague vectors and reservoir

A

Vector = rat flea (xenopsyllia cheopis)

Reservoir = rattus rattus (black), rattus norvegus (brown), other small mammals

174
Q

How is plague transmitted?

A

Bubonic plague: bite of infected xenopsyllia cheopis rat flea

Pneumonic plague: inhaled droplet containing yersinia pestis

Consumption / direct contact with infected rat

175
Q

Clinical syndromes of plague (4)

A

Bubonic plague (most common)
Pneumonic plague
Septic plague
Meningitic plague

176
Q

Clinical syndrome bubonic plague

A

Local lymphadenitis in LN draining flea bite

Buboe develops over 1/52. Painful LN +++, enlarged, non fluctuant mass, overlying skin erythematous and fixed

NOT infectious
Mortality 50%

177
Q

Clinical syndrome pneumonic plague

A

Rapidly developing pneumonia + haemoptysis + respiratory failure

Chest signs and CXR usually unremarkable

INFECTIOUS
Mortality ~100%

178
Q

How is plague diagnosed?

A

Buboe aspirate –> smear –> bipolar staining coccobacilli

Buboe aspirate / blood culture

F1 antigen if available

Identification of Yersinia Pestis on blood film (late stage)

179
Q

How is plague managed?

A

Quick quick start IV abx
Streptomycin main stay

(Chloramphenicol, doxy, ciprofloxacin are alternatives)

180
Q

How is plague prevented?

A
  1. Rat control
  2. Flea control
  3. Isolation pneumonic plague patients, droplet PPE (surgical mask)
  4. Identify contacts, doxy / cipro PEP
181
Q

Tularaemia causative organism

A

Francisella tularaemia

Gram -ve intracellular coccobacilli

182
Q

Tularaemia distribution

A

Scandinavia, USA
Northern hemisphere

183
Q

Tularaemia transmission

A

Pneumonic tularaemia: inhaled bunny rabbit (lawnmower :’( </3 )

Glandular tularaemia: deer fly / hard tick / flea bite

184
Q

Tularaemia clinical syndrome

A

Pneumonic: pneumonia

Glandular: ulcer at bite site + regional LN

Conjunctivitis also seen

185
Q

Tularaemia diagnosis

A

History of exposure is key
PCR / serology

186
Q

Tularaemia treatment and prevention

A

Aminoglycoside –> gentamicin

Bite prevention (trousers, DEET)
PPE when dealing with dead animals

187
Q

Relapsing fever causative organism

A

Borrelia species
Spirochete

Louse borne: borrellia recurrentis

Tick borne: borrellia duttoni

188
Q

What are the different types of relapsing fever?

A

LOUSE BORNE
Borrellia reccurrentis
More severe, fewer relapses
Epidemic, seen in areas of poor sanitation and overcrowding eg refugee camps

TICK BORNE
Borrellia duttoni
Less severe, more relapses
Endemic

189
Q

What is the clinical syndrome of relapsing fever?

A

Fever + HSM + myocarditis + epistaxis + CNS involvement (confusion)

Symptoms last ~5 days, resolve, then recur

190
Q

How is relapsing fever diagnosed?

A

Blood film –> giemsa –> spirochetes ++

PCR great, serology rubbish

191
Q

How is relapsing fever treated?

A

10 days doxycycline
One dose often effective

Beware Jarisch Herxheimer

192
Q

How is relapsing fever prevented?

A

LOUSE BORNE
Improve sanitation
Wash clothes and bedding at 60 degrees

TICK BORNE
Bite prevention

193
Q

Q fever causative organism

A

Coxiella burnetti

Pleomorphic, coccobaccili, poorly staining but gram -ve

Phase variation:
1 = infective, 2 = less infective

194
Q

How is Q fever transmitted?

A
  1. Inhaled aerosol (can travel great distances)
  2. Ingestion unpasteurised milk
  3. Direct contact with animal products, eg POC, carcass, wool
  4. Tick bite
195
Q

What is Q fever clinical syndrome?

A

Mostly asymptomatic / self limiting URTI

ACUTE:
Pneumonia / hepatitis / aseptic meningoencephalitis

CHRONIC:
Culture negative endocarditis
Glomerulonephritis, Guillain Barre, spontaneous abortion

196
Q

How is Q fever diagnosed?

A

Acute and convalescent serum.

Acute Q fever: Phase 2 > phase 1
Chronic Q fever: Phase 1 > phase 2

PCR of liver biopsy / heart valve in reference lab

197
Q

How is Q fever managed?

A

ACUTE: 10/7 doxy

CHRONIC: 18 months (!!) doxy + hydrochloroquine to prevent antiphospholipid syndrome

198
Q

How can Q fever be prevented?

A

Pasteurise milk

Correct handling animal products incl POC, carcass, wool

PPE for those at risk (masks)

Limited vaccine availability for humams

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