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YR5 Microbiology > Crash course: Zoonoses > Flashcards

Crash course: Zoonoses Flashcards

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Biology 101 flashcards
1
Q

What causes Brucellosis? What is it contracted from? When does it present?

A

Brucella spp.
Contracted from raw dairy + farm animals
After 2w incubation

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2
Q

Give 3 features of brucellosis presentation

A

Sudden onset high fever, rigours, headache, malaise, myalgias

Back/ joint pain, hepatosplenomegaly, FLAWSy

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3
Q

Which 2 ‘buzzword’ symptoms are associated with brucellosis

A

BACK PAIN as causes epidural abscess

EPIDIDYMO-ORCHITIS

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4
Q

Give 3 serious manifestations of brucellosis

A

Endocarditis
Osteomyelitis
CNS infection

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5
Q

What is used to diagnose and treat Brucellosis?

A

Dx: Cultures

Tx: Doxycycline + Streptomycin

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6
Q

What causes Rabies? How is it contracted? When does it present?

A

Various Lyssaviruses
Contracted from animals: dogs + bats
After 1-3m incubation

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7
Q

How does rabies present?

A

Initially: fever, headaches, malaise

Within days affects CNS: furious + dumb rabies

Excessive salivation, hydrophobia

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8
Q

How is rabies diagnosed?

A

Often clinically
Dx: Fluorescent antibody test
CSF PCR possible (bad sign)
Biopsy from nape of neck

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9
Q

What is pathogonomic for rabies?

A

Negri body on histology
(inclusion body in infected neurons)

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10
Q

How is rabies treated?

A

Only before symptomatic

If bitten: pre-emptive rabies vaccine + immunoglobulins

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11
Q

What causes plague? What is it contracted from? When does it present?

A

Yersinia pestis
Rat fleas
After hours- couple of days

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12
Q

Give 4 features of bubonic plague

A

Fevers
Rigors
Buboes: massive LNs, when aspirated contain dense black fluid
Dry gangrene

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13
Q

Give 4 features of pneumonic plague

A

Fevers
Rigors
Cough + bloody sputum
ARDS

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14
Q

Give 4 features of septicaemic plague

A

Fevers
Rigors
DIC
Peripheral gangrene

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15
Q

How is plague diagnosed and treated?

A

Dx: Microscopy, culture or PCR

Tx: Aminoglycosides or Doxycycline

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16
Q

What causes Leptospirosis? What is it contracted from? When does it present?

A

Leptospira spp.
Rat urine
After 1w incubation

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17
Q

What scenario may leptospirosis be contracted in?

A

swimming in lake with rat pee in (stagnant water)

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18
Q

How can leptospirosis present?

A

Fevers, chills, rigors, myalgia, pharyngitis ± haemoptysis

Conjunctival suffusion, jaundice, meningitis

Pulmonary or GI haemorrhages, renal failure, haemolysis

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19
Q

Give 2 buzzword symptoms of leptospirosis

A

JAUNDICE

CONJUNCTIVAL SUFFUSION (Dry conjunctivitis, no exudate)

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20
Q

What causes Bartonellosis? How is it contracted? When does it present?

A

Bartonella henselae
Cat scratches
After 1w incubation

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21
Q

How does Bartonellosis present?

A

Painless erythematous crusted papule at scratch site

Lymphadenopathy proximal to inoculation site

Fevers, malaise

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22
Q

What presentation is pathogonomic for Bartenollosis?

A

Parinaud oculoglandular syndrome:
Conjunctivitis + enlarged LN in front of ear

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23
Q

What causes Lyme disease? How is it transmitted? When does it present?

A

Borrelia spp.
Ixodes tick
After days-weeks incubation

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24
Q

How does early localised Lyme disease present?

A

Erythema migrans, esp. inoculation site
“Bulls-eye” or “target” rash

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25
Q

How does early disseminated Lyme disease present?

A

Fevers
Myalgias
Arthralgias
CNS: headache, meningitis
Cardiac: palpitations, heart block

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26
Q

How does late disseminated Lyme disease present?

A

Arthritis
Skin lesions
Polyneuropathies

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27
Q

How is Lyme disease diagnosed and treated?

A

Dx: Clinically if erythema migrans + exposure or rash biopsy/ serology

Tx: Doxycycline
Ceftriaxone if CNS involvement

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28
Q

What causes Leishmaniasis? How is it transmitted?

A

Leishmania spp.
Sand fly bites

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29
Q

How does cutaneous Leishmaniasis present?

A

Well demarcated lesion at site of inoculation

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30
Q

How does mucocutaneous Leishmaniasis present?

A

Follows cutaneous, destructive lesions around face

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31
Q

How does diffuse cutaneous Leishmaniasis present?

A

Widespread nodular rash

32
Q

How does visceral Leishmaniasis present?

A

Gradual onset fever
Hepatosplenomegaly
Pancytopenia

Die of secondary infections if not treated

33
Q

How is Leishmaniasis diagnosed and treated?

A

Dx: Microscopy

Tx: Amphotericin B (for visceral- the form that will kill)
Cutaneous harder to treat

34
Q

What causes Anthrax? What is it found in? How is it spread?

A

Bacillus anthracis
Found in farm/ wild animals
Spread by spores in hair

35
Q

What are the 3 major forms of presentation of Anthrax?

A

Cutaneous
GI
Pulmonary

36
Q

How does cutaneous Anthrax present?

A

Boil that develops into an eschar
Lymphadenopathy

37
Q

How does GI Anthrax present?

A

Haemorrhage necrotic ulcers
Lymphadenopathy
Perforation

38
Q

How does pulmonary Anthrax present?

A

Chest pain
Haemoptysis
SOB
Haemorrhagic mediastinitis

39
Q

What is an eschar?

A

Painless necrotic skin lesion
Deep, dark, black

40
Q

What 2 buzzword symptoms/ signs are associated with anthrax?

A

Eschars
Widened mediastinum

41
Q

List 4 dermatophytoses that can be treated topically

A

Tinea pedis – Athletes foot
Tinea cruris – Groin
Tinea corporis – Body
Tinea manuum – Hands/ palms

42
Q

Give 2 dermatophytoses that require systemic treatment

A

Tinea capitis – Scalp/ hair
Tinea unguium – Finger/ toenails

43
Q

Name 1 organism causing Tinea infection

A

Trichophyton rubrum

44
Q

What causes Pityriasis versicolor? How does this present?

A

Malassezia furfur

Multiple brown/ tan/ hypopigmented lesions across trunk, abdo + face

45
Q

What is the treatment for Pityriasis versicolor?

A

Ketoconazole 2% shampoo

46
Q

What are 2 topical treatments for tinea infections?

A

Clotrimazole 1%
Terbinafine 1%

47
Q

What are 2 oral treatments for tinea infections?

A

Itraconazole
Terbinafine

48
Q

What causes candidiasis?

A

Candida spp.

49
Q

How does candidiasis most commonly present?

A

Vaginal candidiasis (thrush)
+ skin infections

50
Q

Which population is oral candidiasis associated with?

A

Asthmatics- use steroid inhalers (thus encourage to wash mouth out after use)

51
Q

Which population is oesophageal candidiasis associated with?

A

Severe immunosuppression- HIV

52
Q

Which population is disseminated candidiasis associated with?

A

Those with a central line

53
Q

What tests are diagnostic of candidiasis?

A

Beta-D-glucan +ve

Galactomannan -ve

54
Q

How can severe candidiasis be treated?

A

Amphotericin B

55
Q

What causes Aspergillus?

A

Aspergillus spp

56
Q

What is an aspergilloma? In which patients are these seen?

A

Ball of aspergillus that forms in pre-exisiting cavity
Occur in patients with pre-existing cavity e.g. TB, squamous cell lung cancer, bronchiectasis

57
Q

What does invasive aspergillosis involve? In which patients does this occur?

A

Pulmonary + extra pulmonary

Immunocompromised/ those with a line infection

58
Q

What is allergic bronchopulmonary aspergillosis?

A

Hypersensitivity reaction to colonisation
Seen in asthmatics, profound inflammatory response
NOT infection with aspergillus

59
Q

What tests can be used to detect aspergillus?

A

Beta-D-glucan: +ve
Galactomannan: +ve

60
Q

What is the treatment for aspergillosis?

A

Aspergilloma: Surgical removal

Invasive aspergillosis: Amphotericin B

ABPA: Prednisolone

61
Q

What causes sporotrichosis? How is it contracted?

A

Sporothrix schenckii
Contracted from ROSE THORNs- seen in gardeners/ farmers

62
Q

Describe presentation of sporotrichosis

A

Proximally spreading nodular necrotic rash from inoculation site

Can disseminate, producing abscesses in bone, joints, CNS

63
Q

What causes Mucormycosis? In which patients is it seen?

A

Rhizopus + Mucor spp.
Patients that had covid esp. diabetics

64
Q

Describe presentation of Mucormycosis

A

Rhinocerebral infection, necrotic, destroys tissue
Vascular invasion follows
Very high mortality

65
Q

What is PrPc? What is its secondary structure?

A

Protein expressed on surface of neurones of brain
2 structure: Alpha-helical

66
Q

What can PrPc misfold into? What causes this? What does this cause?

A

PrPSc: change in secondary structure: beta pleated sheets

Sporadically, familially or infectiously

Difficult to degrade, water-insoluble, forms big lumps of protein.
Accumulation results in neuronal cell death

67
Q

How does PrPSc interact with normal PrPc?

A

PrPSc can make PrPc misfold
= propagation of protein that can’t be moved or degraded + are neurotoxic

68
Q

What is the most common form of prion disease?

A

Creutzfeldt-Jakob disease

69
Q

What are the 3 forms of CJD?

A

Sporadic: 85% = unknown endogenous cause

Familial: 5-15% = genetic mutation

Acquired: <1%

70
Q

How can CJD be acquired?

A

Acquires first dose of misfolded protein exogenously

Iatrogenic: thus surgical instruments must be autoclaved

Variant: acquired from eating beef with mad-cow disease (prion disease)

71
Q

What is the proper name for mad cow disease?

A

bovine spongioformencephalopathy

72
Q

How is CJD diagnosed?

A

Clinically + supported by imaging

Can only be confirmed on biopsy postmortem

73
Q

In which form of CJD can an alternative investigation be used to diagnose?

A

variant CJD
Prion protein found in tonsils
Ix: Tonsillar biopsy

74
Q

Other than CJD, name 3 prion diseases

A

Kuru

Gerstmann-Sträussler-Scheinker disease

Fatal Familial Insomnia

75
Q

What is Kuru disease?

A

Prion disease seen in Papau New Guinea

Spread through ritual cannibalism

76
Q

What is Gerstmann-Sträussler-Scheinker disease?

A

Autosomal DOMINANT familial prion disease
Slower progression than others
Life expectancy 5y

77
Q

What is Fatal Familial Insomnia?

A

Autosomal DOMINANT familial prion disease
Features prominent insomnia, paranoia, hallucinations

YR5 Microbiology (23 decks)

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