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DTM&H > Non-Malarial Fevers and other IDs > Flashcards

Non-Malarial Fevers and other IDs Flashcards

1
Q

What is the causative organism of Mellioidosis?

A

Psuedomallei Burkholderia

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2
Q

How do you manage Mellioidosis?

A

Ceftazidime 14/7 + 3/12 of co-trimoxazole for eradication

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3
Q

How do you diagnose Melioidosis?

A

Blood Culture
*** Notify the labs because this requires special lab management due to infectiousness

+ Abdo USS –> look for infection elsewhere
+ CXR –> to look for infection elsewhere

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4
Q

What is the bacteriology of P. Burkholderia?

A

Gram-negative environmental bacterium

Found in soil

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5
Q

What is the epidemiology of Meliodosis?

A

South East and South Asia
Australia
Associated with rainy season
Associated w/ Rice Farmers

**3rd most common cause of death in Thailand after HIV and TB

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6
Q

Name five causes of fever that might not grow on blood culture (or be difficult to grow)

A
  • Leptospirosis
  • Rickettsia
  • Brucella
  • Non-malaria blood parasites
  • Mycobacteria, esp MTB
  • Viruses
    *Arbovirus
    *VHF
    *Influenza
    *Fungi
    *Histoplasma
    *Penicillium marneffei
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7
Q

How does the WHO define sepsis?

A

WHO adult sepsis definition
Suspected infection, SBP ≤ 90
mmHg AND 1 of the following:
* HR > 100 bpm
* RR > 24 br pm
* Temp < 36 or >38

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8
Q

What fluid resus is appropriate in adults with sepsis?

A

30ml/kg for crytalloid over 3 hours

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9
Q

Does the WHO recommend SIRS or qSOFA to quantify Sepsis?

A

SIRS

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10
Q

Does the WHO recommend SIRS or qSOFA to quantify Sepsis?

A

SIRS

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11
Q

How does Anthrax lesion present?

A

The anthrax lesion begins as a painless papule that lasts 1 to 2 days before becoming a vesicle that later ruptures. It then develops the classic necrotic central ulcer and may be surrounded by smaller peripheral vesicles. Therefore a patient may present with a non-specific localized papulovesicular eruption.

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12
Q

What causes Anthrax?

A

Bacillus Anthracis

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13
Q

Explain the bacteriology of Bacillus Anthracis

A

Gram +ve rod
Spore Forming

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14
Q

How does anthrax spread to people?

A
  1. Zoonotic Spread
    Many places have zoonotic endeminicity of anthrax
    Asia, Africa, Australia, USA
  2. Bioterrorism
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15
Q

What are the three forms of Anthrax presentation?

A

Cutaenous (95%)
Gastrointestinal
Inhalation

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16
Q

How does cutenous Anthrax present?

A

Vesicular rash –> necrotic eschar

Surround tissue oedema

Malaise

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17
Q

What is the differential for cutaenous anthrax?

A

bacterial ecthyma
rickettsial diseases - Scrub typhus etc.
rat-bite fevers
necrotic arachnidism (Spider bite) ulceroglandular tularaemia
bubonic plague.

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18
Q

How do you diagnose anthrax?

A

Combo of: Gram stain, culture, serology is the TRIFECTA.

HOWEVER -ve culture does not rule out anthrax and you should also do a PUNCH BIOPSY of the lesion

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19
Q

How do you manage Cutaenous Anthrax?

A

10/7 of quinolone or doxy

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20
Q

How long should you treat inhaled anthrax/exposure after bioterrorism?

A

60 days!!!!!!!!!!!!!!

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21
Q

What are the risk factors for Mellioidosis?

A

Exposure to soil and surface water
in endemic area
Diabetes mellitus
Alcohol excess (Australia)
Thalassaemia major
Immune suppression (corticosteroid use)
Cancer
Renal failure and kidney stones

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22
Q

How does Mellioidosis present

A

Sepsis

Basically suspect in any sepsis that does NOT INCLUDE ENDOCARDITIS OR MENINGITIS.
Pulmonary system most often affected, urinary rare but could definitely still be in your differential of urosepsis

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23
Q

What are the two presentations of Melioidosis?

A

ACUTE:
Most commonly bacteraemia and/or multifocal pneumonia.

Often associated with abscesses of the liver and spleen.

Mortality 10 to 50% (depends on level of supportive care available).

CHRONIC:
Chronic melioidosis (~15% of cases)
Most commonly a solitary cold abscess (anywhere in the body).
Frequently mistaken for TB. Survival is the norm.

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24
Q

How is Meliodosis diagnosed?

A

**challenging to diagnose

**microbiological diagnosis; clinical diagnosis is NOT sufficient

** classic ‘safety pin’ sign on gram stain (gram -ve)

In all Patients, sample:
- blood
- urine
- throat swab / rectal swab

WARN THE LAB

Culture on Ashdown agar plate

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25
Q

What antibiotic resistance pattern is seen in melioidosis?

A

‘Gentamicin resistant but sensitive to co-amoxiclav’

**this is important because Burkoholderia Pseudomallei looks very similar to pseudomonas on culture, but pseudomonas is often gent sensative but co-amox resistant

SO if you get this report form the lab then suspect you have melioidosis

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26
Q

How do you treat melioidosis?

A

INITIAL:
Ceftazidime 150mg/kg QID for at least 10 days + absence of fever for 48h

ERADICATION:
Cotrimoxazole (weight based) for 12-20 weeks.

Risk of relapse w/out eradication is 25%

B. pseudomallei is intrinsically resistant to many first line antibiotics!!!!

If you don’t think of melioidosis, then you have a 90% chance of getting the empirical antibiotic choice wrong!!

In endemic settings, failure to respond to broad spectrum antibiotics such as ceftriaxone is
a reason to suspect melioidosis and empirical ceftazidime should be started

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27
Q

Your patient with suspected melioidosis gets started on Ceftazidime. On day 3 you do a liver USS and note that patient has developed a new collection in their liver.

How should you proceed?

A
  1. Keep the current antibiotic regime
  2. Large, accessible collections should be drained, but multiple small abscesses in the liver and spleen need not be drained (and it may be dangerous to do so, if
    radiological guidance is unavailable).

!!!!It is common for collections to grow / enlarge while on appropriate therapy. It is common for patients to develop new
lesions while on appropriate therapy

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28
Q

What education should all melioidosis patients be given upon successful completion of treatment/discharge home?

A

Relapse rate of 5% despite carriage elimination

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29
Q

Name 5 diseases caused by Spirochetes

A
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30
Q

What is Yaws?

What is Bejel?

What is Pinta?

A

A series of spirochete infection causing skin diseases which can resemble syphilis (same family) and have 4 stages of disease if untreated

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31
Q

What is the bacteria responsible for Yaws?

Bejel?

Pinta?

A

Y: Treponema Pallidum Pertenue

B: Treponema Pallidum Endemicum

P: Treponema carateum

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32
Q

Where does Yaws occur?

Bejel?

Pinta?

A

Yaws: Hot humid climates (does not spread well in dry/cold)

South America
Thailan, Indonesia, India, Papua New Guinea have current outbreaks

Bejel: Central and outh Africa, Middle East, Turkey, Burkina Faso

Pinta: South and Central America

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33
Q

Which age group does Yaws affect?

Bejel?

Pinta?

A

Yaws = children <15

Bejel = anyone, F>M, maternal to child transmission via breastfeeding is commonly mentioned

Pinta = Young adults

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34
Q

Which of these disease (Yaws, Bejel, Pinta) causes skin damage only, with NO other organ dysfunction?

A

Pinta (painted skin)

35
Q

Which of these disease (Yaws, Bejel, Pinta) causes bone and cartilage damage, but no other organ damange?

A

Yaws

36
Q

Which of these disease (Yaws, Bejel, Pinta) causes bone, cartilage, eye, cardiac and neuro damage?

A

Bejel

37
Q

How do you diagnose Yaws/Pinta/Bejel?

A

Syphilis Serology
Dark Field Micrscopy
IgM/IgG

38
Q

How do you treat Yaws / Bejel / Pinta?

A

IM Benzathine Penicillin 2.4U IM STAT

39
Q

What organism causes Leptospirosis?

A

Leptospira interrogans

40
Q

How does Lepto spread to humans?

A

Normally found in rodents (and also sheep, cow, dogs etc), and is excreted in their urine.

Human become infected when they come into contact with the urine when it enters through broken skin or mucous membranes

41
Q

What are the phases of Leptospirosis?

A
  1. ASYMPTOMATC
  2. LEPTOSPIRAEMIC PHASE (septicaemia)
    - muscle pain (esp. backs of legs)
    - fever, rigors, weakness
  3. LEPTSPIRURIC PHASE (immune mediated)
    - immune attack aganinst spirochetes: FEVER ±renal/eye/hepatic/CNS invovlement
42
Q

Lepto can present as anicteric or icteric. Describe both of these clinical syndromes

A

Anicteric:
- Aseptic meningitis in 50% of patients, usually for a few days
- Cranial nerve palsies / encephalitis (LOC is pretty uncommon)
- Mild delirium also seen.
- Death is extremely rare in anicteric cases

Icteric:
* Abdominal pain with diarrhoea or constipation (30%), hepatosplenomegaly, nausea, vomiting, and anorexia.
* Uveitis (2-10%) can develop early or late in the disease. Reported as late as 1 year after initial illness.
* Subconjunctival haemorrhage most common ocular complication >90%
* Renal symptoms, hematuria, proteinuria, oliguria 50%
* Pulmonary manifestations occur in 20-70%
* Adenopathy, rashes, and muscular pain also are seen

43
Q

What is Weil Syndrome?

A

A complication of Lepto:

Jaundice, renal dysfunction, hepatic necrosis, pulmonary dysfunction, and hemorrhagic diathesis. (<5%)

44
Q

Give 5 differentials for Lepto

A

Dengue
Hantavirus
Viral hepatitis
Malaria
Meningitis
EBV and CMV
HIV
Rickettsial disease
Typhoid fever

(not exhaustive list)

45
Q

How do you diagnose lepto?

A

Culture (hard to grow anything)
MAT ELISA IgM (Gold standard! Look for a 4 fold increase!)
Antibody test

RDT in the works but not available yet

46
Q

How do you manage Lepto?

A

Mild leptospirosis: doxycycline, amoxicillin.

Severe leptospirosis: parenteral
penicillin/cephlosporins or erythromycin

Doxycycline prophylaxis weekly for short term
exposures

Vaccination if very high risk (ie. regularly work with rats)

47
Q

How can you prevent lepto?

A

Control of livestock infection with good sanitation, immunization.

Preventing animals from urinating in waters where humans have contact.

Disinfecting contaminated work areas.

Providing worker education.

Protective equipment when handling infected animals or tissues

Public health measures:
Case finding in suspected outbreaks.
Implementing control measures: identify infected area and avoid entering water and leisure activities

48
Q

What is Brucellosis?

A

A gram negative infection causing chronic fever and anorexia

49
Q

Name three bacteria implicated in Brucellosis

A

Brucella Abortus
Brucella suis
Brucella Melitensis

50
Q

How is brucella transmitted?

A

Aerosolised
Ingested (goats milk classically)

51
Q

What kind of bacteria is Brucellla

A

Gram negative cocobacillus

52
Q

Where might you find Brucellosis?

A

Mediterranean, middle east, north africa

53
Q

How does brucellosis present?

A

Intermittent fever, often over several months
Anorexia
Weight loss
Faget’s sign
GI symptoms
Arthralgia

OTHER:
- spinal disease: back pain, painful discs, vertebral involvement (L4)
- monoarthrtis
- orchitis

54
Q

What are the clinical Syndromes of Brucellosis?

A
  1. Asymptomatic
  2. Acute < 1month
  3. Subacute/relapsing 1-6 months
  4. Chronic > 6 months
  5. Hypersensitivity
    Also consider focal symptoms
55
Q

How is brucellosis diagnosed?

A

Agglutination test
(Re: Prozone effect, whereby in very high cases of antibody the agglutination test might actually be NEGATIVE! beware flase negatives)

Culture - Blood, CSF

56
Q

How do you manage Brucellosis?

A

Uncomplicated:
6 weeks of two Abx:

Doxy +streptomycin (gold standard)

OR

Doxycycline + Rifampicin

If chronic or complicated (e.g. bony involvement) treat for 3 months

57
Q

How often should you follow up your Brucella patients?

A

3 monthly for the first year

**relapse is likely to occur in the first 3 months

58
Q

How do you manage brucellosis in children?

A

<8 y/old:
* gentamicin 5 days
* cotrimoxazole 3 weeks

≥8 y/old
* gentamicin 5 days
* doxycycline 3 weeks

59
Q

How can you prevent brucellosis?

A

Improved husbandry
encourage milk pasteurisation
Encourage cessation of consumption of raw liver
Vaccinate animals
Test and Trace + PEP (Doxycycline)

60
Q

What bacteria is respobsible for Anthrax?

A

Bacillus anthracis

61
Q

What bacteria are considered highly dangerous ‘group 3’ pathogens, which you must inform the labs of before you send?

A

Bacillus anthracis
Brucella abortus
Brucella canis
Brucella melitensis
Brucella suis
Burkholderia pseudomallei
Coxiella Burnetti
Rickettsia Typhi (mooseri)
Salmonella Typhi/paratyphi
Shigella dysinteriae
Yersinia Pestis

62
Q

Describe the bacteriology of Anthrax

A

Gram positive rod,
usually squared ends
‘Safety pin’ appearance
Spore forming

63
Q

How does anthrax spread

A

Cutaenous - spores enter into broken skin

Gastro - bacteria is consumed from infected food

Pulmonary - inhalation of spores; most often secondary to biothreat

64
Q

How does cutaenous anthrax present?

A

Ulcerating lesion with significant peri-odema and a vesicle ring –> after several days develops into an eschar

65
Q

How does gastro anthrax present?

A

Rare, maybe underdiagnosed

orpharyngeal ulceration and odema

intestinal oedma, pain, ascites, peritonitis, shock

mortality >80%

66
Q

How does pulmonary anthrax present?

A
  • Haemorrhagic
    adenopathy/mediastinitis
  • Pleural effusions
  • Bacteraemia
  • Meningitis will accompany
    as disease progresses
67
Q

How do you manage anthrax?

A

CUTANEOUS:
60 days of Doxycycline or ciprofloxacin

GASTRO/INHALATION:
60 days of doxycycline or ciprofloxacin PLUS rifampicin, chloramphenicol or clindamycin

68
Q

What PEP should you use in anthrax?

A

Cipro or doxy for 30/7

±

Vaccine (currently used by british and american military)

69
Q

What bacteria causes Plague?

A

Yersinia pestis

70
Q

How does plague spread (i.e. what is the vector?

A

Oriental/Tropical Rat Flea

Xenopsylla

(also guinea pigs in peru and camels in the middle east and chipmunks in USA)

71
Q

What are the three main Biovars of plague?

A

Orientalis
Antiqua
medievalis

72
Q

What 3 clinical forms of plague are there?

A

Bubonic
Pneumonia
Septicaemic –> disseminated; causes symptoms anywhere including GI and CNS

73
Q

Which form of plague can be spread from person to person?

A

Pneumonic Plague

74
Q

How can you manage plague?

A

ANTIBIOTICS AND SUPPORTIVE CARE

Cipro, Levo, moxiflox, streptomycin, doxy all useful

75
Q

How does Bubonic plague present?

A
  • Incubation 2-7 days
  • Malaise
  • High fever
  • Pain or tenderness over lymph nodes, enlarge to be called buboes
    • Groin is the most common site
  • Bacteraemia initially intermittent then constant.
  • DIC
  • Shock/Convulsions

**death occurs within 2-4 days

76
Q

What is the pathophysiology of bubonic plague?

A

Enters into the skin from a flea bite –> taken up by macrophages –> enters into lymph nodes where bubo forms –> if untreated leads to lymphatic necrosis and haemoatongenous spread to other locations –> GIT, CNS etc.

77
Q

What is the CFR of untreated plague?
- Pnuemonia
- Bubonic

A

Pneumonic: 100% CFR if unterated
Bubonic: 66% if untreated, 13% if treated

78
Q

How does Pulmonary plague spread?

A

Large droplet spread
**The only form of plague that is tranmissible from human to human

79
Q

How does pulmonic plague present?

A
  • Fever, lymphadenopthy, cough, chest pain, haemoptysis
  • CXR: patchy bronchopneumonia, cavities or confluent consolidation
  • Sputum purulent and contains bacilli.

-100% mortality without treatment. 50% with (CDC)

80
Q

How do you diagnose plague?

A
  1. Bubo aspirate –> microscopy and culture: Small gram negative Cocobacilli
  2. Bloods: thrombocytopenia, deranged LFTs and U+Es, neutrophilia
  3. Yersinia Pestis F1 antigen
81
Q

How do you treat plague?

A

Supportive
Antibiotics
Streptomycin im 30mg/kg 2 doses daily 10days

But: limited availability, side effects-renal, hearing.

**penicllins really do not work

82
Q

How can you prevent Plague outbreaks?

A
  1. vaccine in high risk groups
  2. PEP (co-trimoxazole, as per, in high risk groups)
  3. Flea control
  4. Rat control
83
Q

What are the case definitions for a Plague Outbreak?

A
84
Q

What guidelines might help you manage a septic patient in an LMIC?

A

Follow WHO IMAI or SSC guidelines (guideline for the management of poorly patients with limited resources)

DTM&H (29 decks)

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