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Liv Path > Microbio - Niche Infections and the Globo Ones > Flashcards

Microbio - Niche Infections and the Globo Ones Flashcards

1
Q

Rapid neurological degeneration with normal Ix think

A

Prion disease

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2
Q

Type of encephalopathy in prion disease

A

Spongifom

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3
Q

Prion protein - normal and changes in disease

A

Prion protein gene on chromosome 20 - mainly expressed in CNS
When it is in a-helical structure it is protease sensitive, however when it is in the b-pleated sheet configuration it is not.

Prion disease promotes irreversible conversion from a-helical to B-pleated sheet.

Trigger remains unclear in sporadic cases.

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4
Q

Prion Disease Classification

A

Sporadic:
Creutzfeldt-Jakob Disease (80%)

Acquired (<5%):

  • Kuru
  • variant CJD
  • iatrogenic CJD: GH, Blood, Surgery

Genetic (15%):
PRNP mutations
eg. Gerstmann-Straussler-Sheinker syndrome, Familial Fatal Insomnia

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5
Q

Sporadic CJD - presentation, epi, causes

A

Rapid dementia with: myoclonus, cortical blindness, akinetic mutism, LMN signs

Mean age onset 65 yrs (range 45-75 yrs)

Incidence 1/million/year

Death within 6/12

Cause uncertain

  • ? somatic PRNP mutation
  • ? spontaneous conversion of PrPc to PrPsc
  • ?? Environmental exposure to prions
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6
Q

Sporadic CJD - Diagnosis

A
  • EEG - periodic, triphasic complexes (non-specific), 2/3 abnormal
  • MRI- basal ganglia – increased signal
    cortical/striatal signal change on diffusion weighted imaging MRI
  • CSF increased 14-3-3 protein, S100 (markers of neuronal damage)
  • Neurogenetics to r/o genetic cause
  • Tonsillar biopsy NOT useful
  • Brain biopsy
  • Autopsy – by experienced pathologist - spongiform vacuolation and PrP amyloid plaques
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7
Q

Sporadic CJD - Differentials

A 
Alzheimer’s disease
Vascular dementia
Mixed dementia (AD + vascular)
CNS neoplasm eg. glioma, metastases
Cerebral vasculitis
Paraneoplastic syndrome
Familial CJD
vCJD
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8
Q

Variant CJD - Background

A
  • Atypical CJD in teenagers and young people
  • First reported in 1990s in 1990s
  • Thought to link to mad cow disease (BSE)
  • Younger age of onset (median age 26 yrs)
  • Median survival time 14 months
  • Psychiatric onset: dysphoria, anxiety, paranoia, hallucinations
  • Then neurological: peripheral sensory symptoms, ataxia, myoclonus, chorea, dementia
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9
Q

vCJD- Diagnosis

A
  • MRI brain - positive pulvinar sign (bilateral FLAIR hyperintensities involving the pulvinar thalamic nuclei)
  • EEG – non-specific slow waves
  • CSF – 14.3.3, S100 not useful
  • Neurogenetics (almost 100% are MM at codon 129 so far)
  • Tonsil biopsy 100% sensitive and specific –> eliminates need for further investigation to exclude other treatable causes, important for therapeutic trials and early treatment. May be positive in incubation period prior to clinical onset. See FLORID PLAQUES.
  • (Brain biopsy)
  • Autopsy
  • PrPSc type 4t detectable in CNS + most lympo-reticular tissues
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10
Q

Iatrogenic CJD - Causes

A

Human cadaveric growth hormone

Corneal transplants

Neurosurgical procedures eg. dural grafts, pre-1991

Blood transfusions, other blood products

Other surgical procedures? - appendicectomy and tonsillectomy in vCJD

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11
Q

Iatrogenic CJD - Clinical Features

A

Progressive ataxia initially

Dementia and myoclonus later stages

Speed of progression depends on route of inoculation (CNS inoculation fastest)

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12
Q

Prion Genetics

A

3 Aspects:

Codon 129 polymorphism

  • Methionine – Methionine (MM) - found in nearly 100% of vCJD
  • Methionine – Valine (MV)
  • Valine – Valine (VV)

Specific PRNP mutations (~30 so far, all AD)

Consider other neuro-genetic conditions eg. Huntington’s, spinocerebellar ataxia

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13
Q

Familial Prion Disease - GSS, FFI, CJD

A

Fix is crucial: dementian, “MS”, ataxia, psych

  • EEG - non-specific
  • MRI - basal ganglia: sometimes high signal
  • Neurogenetics crucial
  • If -ve: SCA, Huntington’s
  • Autopsy
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14
Q

Familial Prion Disease - GSS(Gerstmann-Straussler-Scheinker syndrome)

A

Slowly progressive ataxia

Diminished reflexes

Dementia

Onset age 30-70 years

Survival 2-10 years

PRNP P102L, but several other mutations

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15
Q

Familial Prion Disease - Familial Fatal Insomnia (FFI)

A 
Untreatable insomnia --> psych issues 
Dysautonomia
Ataxia
(thalamic degeneration)
PRNP D178N +/ pyramidal/extrapyramidal signs, late cognitive decline
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16
Q

Kuru

A

Longest incubation - up to 45 years
From endocannabolism
Progressive cerebellar syndrome –> death within 2 years
Dementia late or absent

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17
Q

CJD Treatment

A

Symptomatic: clonazepam – mycolonus (can also give valproate, levetiracetam, piracetam)

Delaying prion conversion:

  • quinacrine
  • pentosan (intra-ventricular administration)
  • tetracycline

Anti-prion antibody (prevents peripheral prion replication and blocks progression to disease in infected mice but does not get into CNS)

Depletion of neuronal cellular prion protein (prevents onset of disease in mice and blocks neuronal cell loss + reverses early spongiosis)

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18
Q

Fungi - Types of Yeast

A

Candida
Cryptococcus
Histoplasma (Dimorphic)

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19
Q

Fungi - Types of Moulds

A

Aspergillus
Dermatophytes
Agents of mucormycosis

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20
Q

Candida - Gram Stain

A

+ve budding yeast

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21
Q

Candidiasis

A

Primary or secondary mycotic infection caused by members of the genus Candida.

Clinical manifestations:

  • Acute, subacute or chronic, episodic.
  • Involvement may be localized to the mouth, throat, skin, scalp, vagina, fingers, nails, bronchi, lungs, or the gastrointestinal tract, or become systemic as in septicaemia, endocarditis and meningitis.

Distribution: World-wide.

Aetiological Agents: Candida albicans, C. glabrata, C. tropicalis, C. krusei. C. parapsilosis, C. guilliermondii and C. pseudotropicalis.
All are ubiquitous and occur naturally on humans.

Screening test for C. albicans - characteristic germ tubes on fluorescence?

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22
Q

Candida Endophtalmitis

A
  • Often associated with candidemia, indwelling catheters or drug abuse, however it is rare in patients with severe neutropenia.
  • Lesions are often localized near the macula and patients complain of cloudy vision.
  • Exogenous Candida endophthalmitis is rare, but cases have been reported following ocular trauma or surgery.
  • Similarly, conjunctival and corneal infections have also been recorded following trauma.
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23
Q

Chronic oral candidiasis

A
  • Tongue and mouth corners (angular cheilitis)
  • Suggests underlying immune deficiency.
  • Characteristic white pseudomembrane composed of cells and pseudohyphae of C. albicans.
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24
Q

Stain for invasive candidiasis postmortem

A

Periodic Acid-Schiff (PAS) stained section.

Blastoconidia and branched pseudohyphae.

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25
Q

Candidiasis - Diagnosis

A
  • Blood cultures for candidaemia, other samples for short term fungal culture.
  • B D Glucan assay (serology)
  • Imaging e.g. for hepatosplenic candidaisis
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26
Q

Candidiasis - Rx

A
  • At least 2 weeks of antifungals from first negative blood cultures.
  • ECHO and fundoscopy
  • Echinicandin empirically and for non-albicans Candida
  • Fluconazole for Candida albicans
  • Ambisome (e.g. CNS), Fluconazole (e.g. urine) or Voriconazole (e.g. CNS) for organ-based disease.
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27
Q

Cryptococcosis

A
  • Chronic, subacute to acute pulmonary, systemic or meningitic disease
  • Initiated by the inhalation of the fungus.
  • Primary pulmonary infections have no diagnostic symptoms and are usually subclinical.
  • On dissemination, the fungus usually shows a predilection for the central nervous system, however skin, bones and other visceral organs may also become involved.

Distribution: World-wide.

Aetiological Agent: Cryptococcus neoformans.

Susceptibility greatly increased in pts with impaired T-cell immunity e.g. AIDS (2nd most common cause of death in AIDS)

Life cycle: eucalyptus tree –> bird excreta –> spores –> inhaled –> alveoli –> CNS

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28
Q

Crytococcus neoformans var. gattii

A

Causes a meningitis in apparently immunocompetent individuals in tropical latitudes, esp. SE Asia and Australia

High incidence of space-occupying lesions in brain and lung

Increased resistance to amphotericin B clinically

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29
Q

Cryptococcal Meningitis CSF stain

A

India ink - budding yeast cell surrounded by characteristic wide gelatinous capsule.

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30
Q

Cryptococcomas on MRI appear as

A

discrete white masses

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31
Q

Cryptococcus gattii on agar

A

typical brown colour effect due to phenol oxidase activity.

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32
Q

Cryptococcosis - Diagnosis

A

Diagnosis almost entirely around detection of Cryptococcal antigen in blood or CSF

Typical clinical features

Immunosuppressed host

Often culturable from blood, body fluids

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33
Q

Cryptococcosis - Management

A

3/52 Amphotericin B +/- flucytosine

Repeat LP for pressure management

Secondary suppression with fluconazole

Some evidence that high dose fluconazole effective

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34
Q

Aspergillosis - Genera

A
  • Spectrum of diseases of humans and animals caused by members of the genus Aspergillus including:
    (1) mycotoxicosis due to ingestion of contaminated foods
    (2) allergy and sequelae to the presence of conidia or transient growth of the organism in body orifices
    (3) colonization without extension in preformed cavities and debilitated tissues
    (4) invasive, inflammatory, granulomatous, necrotizing disease of lungs, and other organs
    (5) systemic and fatal disseminated disease (rare).
  • The type of disease and severity depends upon the physiologic state of the host and the species of Aspergillus involved.

Distribution: World-wide.

Aetiological Agents: Aspergillus fumigatus, A. flavus, A. niger, A. nidulans and A. terreus.

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35
Q

Aspergillus stain

A

Methenamine silver (GMS) –> fungal hyphae - balls or dichotomously branched

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36
Q

Aspergillosis - Management

A
  • Voriconazole
  • Ambisome
  • Caspofungin/Itraconazole less good
  • At least 6 weeks of therapy
  • Duration based on host/radiological/mycological factors
37
Q

Dermatophyte Infection

A

Tinea

Onchomycosis

38
Q

Tinea pedis - organisms

A

Trichophyton rubrum or T. interdigitale, less commonly by Epidermophyton floccosum

39
Q

Tinea cruris - organisms

A

Groin

T. rubrum and E. floccosum

40
Q

Tinea capitis - organisms

A

T. rubrum and T. tonsurans

41
Q

Onchomycosis - organisms

A

Trichophyton spp, Epidermophyton spp, Microsporum spp.

42
Q

Pityriasis Versicolor - Organisms

A

MALASSEZIA FURFUR

M. sympodialis, M. globosa, M. restricta, M. obtusa, and M. slooffiae

43
Q

Mucormycosis

A

Immunocompromised patients, poorly controlled Diabetes mellitus

Cellulitis of the orbit and face progress with discharge of black pus from the palate and nose.

Retro-orbital extension produces proptosis, chemosis, ophthalmoplegias and blindness.

As the brain is involved, there are decreasing levels of consciousness.

Rhizopus spp, Rhizomucor spp, Mucor spp

44
Q

Mucormycosis - Rx

A

Surgical debridement very important, antifungal: Amphotericin, posaconazole

45
Q

Targets of Antifungal Therapy

A

Cell membrane - Fungi use principally ergosterol instead of cholesterol

DNA Synthesis- Some compounds may be selectively activated by fungi, arresting DNA synthesis.

Cell Wall - Unlike mammalian cells, fungi have a cell wall

46
Q

Antifungals Targeting Cell Wall

A

Polyene antibiotics:

  • Amphotericin B, lipid formulations
  • Nystatin (topical)

Azole antifungals (far less toxic than amphotericin):

  • Ketoconazole
  • Itraconazole
  • Fluconazole
  • Voriconazole
  • Miconazole, clotrimazole (and other topicals)
47
Q

Antifungals Targeting DNA/RNA Synthesis

A

Pyrimidine analogues e.g. Flucytosine

Flucytosine is an anti-metabolite type of antifungal drug. It is a synthetic fluorinated pyrimidine (FC –> FU, humans lack the enzyme that converts this) which is available for intravenous infusion or oral administration.
It is marketed as Ancotil.

Restricted spectrum of activity:
Acquired Resistance- result of mono therapy, rapid onset
Due to:
1) Decreased uptake (permease activity)
2) Altered 5-FC metabolism (cytosine deaminase or UMP pyrophosphorylase activity)

Uses:

  • Monotherapy now limited
  • In combination with amphotericin B or fluconazole for candidiasis, crypto coccus and ?aspergillosis

SEs:

  • Infrequent – include D&V, alterations in liver function tests and blood disorders.
  • Blood concs need monitoring when used in conjunction with Amphotericin B.
48
Q

Antifungals Targeting Cell Wall

A

Echinocandins e.g. Caspofungin acetate (Cancidas)

49
Q

Azoles - MOA

A

In fungi, the cytochrome P450-enzyme lanosterol 14-a demethylase is responsible for the conversion of lanosterol to ergosterol

Azoles bind to lanosterol 14a-demethylase inhibiting the production of ergosterol

Some cross-reactivity is seen with mammalian cytochrome p450 enzymes

  • Drug Interactions
  • Impairment of steroidneogenesis (ketoconazole, itraconazole)
50
Q

Water-Soluble Triazoles

A

Voriconazole - similar structure to fluconazole but WATER SOLUBLE. limited spectrum of activity against fungi but also good oral bioavailablity and tissue penetration.

Structural similarity between azaleas and triazoles predicts that cross-resistance between these drugs is likely to occur.

51
Q

Lipophilic Triazoles

A
  • Posaconazole and itraconazole
  • Not generally detected in CSF - debate re CNS penetration
  • These azoles have extended spectrums of acivity when compared to fluconazole or voriconazole, but their lipophilic nature impairs gastrointestinal absorption
  • Long side chain may help binding of drug to erg11
52
Q

Echinocandin Antifungals

A
  • Target fungal cell wall
  • Caspofungin, micafungin, anidulafungin
  • All have low oral bioavailablility so must be given IV due to large molecular weight
  • All drugs have very similar spectrum of action. Primarily active against candida and aspergillus species.
  • Degraded in the liver and excreted in the bile.
  • Important to note that urine and csf concentrations are negligible.
53
Q

Echinocandins - Pharmacology/MOA

A

Cyclic lipopeptide antibiotics that interfere with fungal cell wall synthesis by inhibition of ß-(1,3) D-glucan synthase.

Loss of cell wall glucan results in osmotic fragility

Spectrum:

  • Candida species including non-albicans isolates resistant to fluconazole
  • Aspergillus spp. but not activity against other moulds (Fusarium, Zygomycosis)
  • No coverage of Cryptococcus neoformans
54
Q

Polyene Antifungals

A
  • Amphotericin B
  • Therapy for systemic fungal infection
  • Binds sterols in fungal cell membrane
  • Creates transmembrane channel and electrolyte leakage –> loss of transmembrane potential –> impaired cellular function
  • Active against most fungi except Aspergillus terreus, Scedosporium spp.
  • Very little resistance despite long use
  • Tendency to form miolecular aggregates which cause red cell lysis and lodge in the renal tubules causing drug reactions and renal impairment (liposomal amphotericin B prevents this by holding the drug in a phospholipid bilyaer - can also get ampB colloidal dispersion and ampB lipid complex)
55
Q

Amphotericin B - Nephrotoxicity

A

Most significant delayed toxicity

Renovascular and tubular mechanisms

  • Vascular-decrease in renal blood flow leading to drop in GFR, azotemia
  • Tubular-distal tubular ischemia, wasting of potassium, sodium, and magnesium

Enhanced in patients who are volume depleted or who are on concomitant nephrotoxic agents

56
Q

Zoonoses - Transmission

A

Every day contact with animals- Scratches or bites

By-products (feces/urine)- Contaminated soil, Litter

Foodstuffs- Carcass processing, Milk and milking, Raw/undercooked meats

57
Q

Cambylobacter

A

Reservoir: Poultry (80% UK cases), Cattle

Transmission: Contaminated food

Clinical presentation: Diarrhoea, Bloating, Cramps

Investigations: Stool culture

Management: Supportive

58
Q

Salmonella

A

Reservoir: Poultry, Reptiles/amphibians

Transmission: Contaminated food, Poor hand hygiene

Clinical presentation: Diarrhoea, Vomiting, Fever

Investigations: Stool culture

Management: Supportive, Ciprofloxacin, Azithromycin

59
Q

Bartonella henselae

A

Reservoir: Kittens > cats

Transmission: Scratches, Bites, Licks of open wounds, Fleas

Causes two diseases:

  • Cat Scratch Disease
  • Bacillary angiomatosis

Bartonella is a slightly curved Gram negative rod. Kittens are more likely to infect people because they scratch more often and have a higher prevalence of Bartonella. Prevalence in cats of all ages can be 30 to 50%.

60
Q

Bartonella henselae - Cat Scratch Disease - Presentation, Ix, Rx

A

Clinical presentation

  • Macule at site of innoculation
  • Becomes pustular
  • Regional adenopathy
  • Systemic symptoms
  • 14% of cases can progress to more severe symptoms which can include eye problems, encephalopathy, arthritis, osteolysis, vascular system lesions, hepatitis, or pneumonia.

Investigations: Serology

Management: Erythromycin, Doxycycline

61
Q

Bartonella henselae - Bacillary angiomatosis - Presentation, Ix, Rx

A

Clinical Presentation

  • Occurs in immunocompromised
  • Skin papules
  • Disseminated multi-organ and vasculature involvement

Investigations: Histopathology, Serology

Management: Erythromycin, Doxycycline, PLUS rifampicin

Mostly in HIV - infected and other immuno-suppressed individuals. Much more severe disease than is CSD.
Vascular lesions may involve many organs, with skin being the most common.
Prevention: Wash hands after handling cats, Use flea control, Do not let cats lick areas of abraded skin or open wounds.

62
Q

Toxoplasmosis

A

Reservoir: Cats, Sheep

Transmission: Infected meat, Faecal contamination

Clinical Presentation

  • Fever
  • Adenopathy
  • Still-birth
  • Progressive visual, hearing, motor, & cognitive issues
  • Seizures
  • Neuropathies

Investigations- Serology

Management- Spiramycin, Pyrimethamine plus sulfadiazine

63
Q

Brucellosis

A

Reservoir: Cattle, Goats

Transmission: Unpasteurised milk, Undercooked meat, Mucosal splash, Aerosolisation/inhalation

Clinical Presentation

  • Fever
  • Back pain
  • Orchitis
  • Focal abscesses (Psoas, liver etc)

Investigations: Blood/pus culture, Serology

Management: Doxycycline PLUS Gentamicin OR Rifampicin

Incubation period- usually 30 days but can be up to 5 months
Symptoms - non-specific. Fever, chills, headache, myalgia, arthralgia, anorexia, fatigue, lymphadenopathy and splenomagaly.
The ratio to subclinical to clinical cases is 1:1 to 12:1.

64
Q

Coxiella burnetii - Q fever

A

Reservoir: Goats, Sheep, Cattle

Transmission:

  • Aerosolisation/inhalation of secretions, waste, or milk of infected animals
  • Unpasteurised milk

Clinical Presentation

  • Fever
  • ‘Flu-like illness
  • Pneumonia
  • Hepatitis
  • Endocarditis
  • Focal abscesses (Para-vertebral/discitis etc)

Investigations: Serology

Management: Doxycycline
(hydroxychloroquine)

65
Q

Rabies (Lyssa virus)

A

Reservoir: Dogs, Cats, Bats

Transmission: Bites, Scratches, Contact with infected fluid

Clinical Presentation

  • Seizures
  • Excessive salivation
  • Agitation
  • Confusion
  • Fever
  • Headache

Investigations: Serology, Brain biopsy, (USA saliva PCR)

Management: Immunoglobulin, Vaccine

66
Q

Rate Bite Fever

A

Reservoir: Rats

Transmission: Bites, Contact with infected urine or droppings

Responsible agents either: Streptobacillus moniliformis or Spirillum minus. Very common carriage.

Clinical presentation

  • Fevers
  • Polyarthralgia
  • Maculopapular progressing to purpuric rash
  • Can progress to endocarditis

Investigations: Joint fluid microscopy & culture, Blood culture

Management: Penicillins

67
Q

Hantavirus Pulmonary Syndrome

A

Reservoir:

  • Deer mouse; Sin Nombre virus
  • White footed mouse; Sin Nombre virus
  • Cotton rat; Black canal virus
  • Rice rat; Bayou virus

Transmission:

  • Contact with infected urine or droppings
  • Aerosolisation

Clinical presentation:

  • Fever
  • Myalgia
  • ‘Flulike illness
  • Respiratory failure
  • May progress to bleeding, renal failure

Investigations: Serology, PCR

Management: Supportive

Western & southern USA and most of central & South America
HPS has also been linked with hypertensive renal disease in the inner city

68
Q

Viral Haemorrhagic Fever

A

Reservoir:

  • Ebola - ? Bats
  • Marburg - ? Bats
  • Lassa – Rats
  • CCHF - ticks

Caused by a number of viruses – Lassa, Marburg, Ebola, and Congo-Crimean Hemorrhagic Fever

Transmission: Contact with fluids of infected

Clinical presentation

  • Fever
  • Myalgia
  • ‘Flulike illness
  • Bleeding

Investigations: Serology, PCR

Management: Supportive

69
Q

Rickettesia

A 
Transmitted via ticks on small rodents. 
“Spotted rocky mountain fever”
Symptoms include: fever, constitutionals and vasculitis. 
Dx = Serology
Tx = Doxycycline.
70
Q

Plague

A 
Organism: Yersinia Pestis
Found on rats, transmitted by fleas
Bubonic – Swollen LNs + Dry gangrene. 
Pneumonic – resp issues and bloody sputum. 
Dx = PCR
Treatment = “plague Causes Dry Gangrene Slowly”
C = Chloramphenicol
D = Doxycline
G = Gentamicin
S = streptomycin
71
Q

Anthrax

A

Organism: Bacillus Anthracis
Cutaneous = painless round black lesion
Pulmonary = mediastinal haemorrhage, pleural effusion, lymphadenopathy
Tx = Doxycycline.

72
Q

Leptospirosis

A

Organism: L. Interrogans (Gm –ve motile spirochaete)
Transmitted from farm animals (urine) or contaminated water (urine).
Symptoms: Constitutionals
Complications: Jaundice, renal issues, myocarditis, uveitis.
Treatment: Doxycyline.

73
Q

Lyme Disease

A

Organism: Borrelia Burgoferia
Transferred via Ixodes tick (lives on deers) therefore associated with hiking.

Symptoms:
PHASE 1 – Erythema chronicum migrans aka Bulls eye rash, and flu like symptoms
PHASE 2 – Malaise, Carditis, Meningitis
PHASE 3 – Neurological signs, and arthriti.
Tx = Doxycycline.

74
Q

Leishmania

A
  • Organism: Unicellular protozoa
  • Spread by sandflies (common in south America, north Africa and the middle east)
  • Dx = Can be cultured on NMN medium (novy-macneal-nicolle) medium.

Signs and symptoms:

  • Visceral aka Kala Azar – Caused by L. Donovani. Can be fatal: Constitutional, Hepatosplenomegaly, BM invasion, Post Kala-azar dermal leishmaniasis (PKDL)
  • Cutaneous (commonest) – caused by L. Major and L Tropica, Scaly ulceration
  • Mucocutaneous – caused by L Braziliensis: Mucous membrane destruction via ulceration, Deforming facial lesions

PKDL= macular, maculopapular, and nodular rash in a patient who has recovered from VL and who is otherwise well.

75
Q

Trypansoma

A

Organism: Flagellate, unicellular protozoa.
Spread by the Tse-Tse fly.
Aka. Sleeping sickness

Signs and symptoms:

  • Constitutionals
  • Sleep Disturbance
  • Neuro issues
  • Lethargy
  • Lymphadenopathy

T. Brucei Gambiense - Gradual infection. Commonest subtype.
T Brucei. Rhodeisiense- Rapid infection
T. Cruzii aka Chagas Disease

76
Q

T. Cruzii aka Chagas Disease

A

Found in Brazil, transmitted by the Reduviid bug.
Acute = “purple eyelids” + constitutionals.
Chronic = Affects the oesophagus, heart and GI tract.

77
Q

Helminths

A

WORMS

Helminths have parasitised humans for millennia

A parasite does not “want” to kill its host

Most worms cause little (if any) damage

When damage occurs, it may be:
oSlow: the worm, or its progeny, attempts to escape
oRapid: tissue damage as humans are not the natural host

Many worms have very complex lifecycles and cannot complete the lifecycle in one host

78
Q

Types of Helminths

A

Cestodes (tape worms)

  • Hydatid
  • Pork / Beef / Fish tape worm

Trematodes (Flukes)

  • Lung, liver, intestinal
  • Blood (Schistosoma)

Nematodes (Roundworms)

  • Hookworms
  • Ascarids
  • Strongyloides
79
Q

Cestodes (tapeworms)

A
  • Beef and pork tape worms are worms of human beings
  • Echinococcus (Hydatid) is a dog tape worm
  • These things cause trouble when humans become an accidental intermediate host
  • Cyst formation in tissues causes mass effect
  • Diagnosis with serology and imaging
  • Treatment is difficult (but not always required)
80
Q

Treatment and Prevention of Cestodes

A

Of worms: easy

  • Praziquantel for human tape worms
  • Praziquantel for dogs (Echinococcus)

Of cysts: difficult
- Hydatid: drugs don’t penetrate –> PAIR, Surgery, long term albendazole, praziquantel

  • Cysticercosis: dying worms cause trouble –> Albendazole, praziquantel and STEROIDS.

Prevention:
- Hygiene, de-worm dogs, cull foxes.

81
Q

Schistosomiasis

A

Probably the most common imported non-GI helminth

4 species, found in Africa, SE Asia and South / Central America

Lifecycle:

  • Cercariae invade human skin when in contact with contaminated water.
  • Worms develop in venous plexus
  • Eggs excreted in faeces or urine
  • Hatch into miracidia, which parasitise snails
  • Snails release cercariae

Adult schistosomes lay eggs:

  • Migration of eggs through bladder or bowel causes damage
  • Retrograde passage of eggs into the liver causes “cirrhosis”
Diagnosis 
Microscopy:
- Urine: S. haematobium
- Stool: S. mansoni, S. japonicum
Serology
Biopsy

Treatment:
Easy - praziquantel

Prevention:
Hard
- Kill snails
- Destroy snail habitat
- Mass treatment
- Interrupt transmission: no swimming, no washing etc.
82
Q

Soil Transmitted Helminths

A

Very well adapted to humans and cause little pathology

3 main pathogens are:

  • Ascaris lumbricoides – ingested with food
  • Trichuris trichiura – ingested with food
  • Hookworm – transdermal infection
  • Plus (special case): Strongyloides stercoralis – transdermal infection

Cause disease through:

  • Migration (ascaris, hookworm and strongyloides)
  • Intestinal obstruction (ascaris)
  • Malabsorption and blood loss (all of them)
  • Psychological distress
83
Q

Strongyloides

A

The only helminth capable of autoinfection

Therefore worm burden not related to infectious dose

Lifecycle:

  • Larvae invade skin
  • Mature into adult pinworms in the small bowel
  • Eggs produced, hatch into rhabtidiform larvae
  • These mature into filariform larvae (infectious)
  • These can autoinfect via perianal skin

Damage:

  • Hyperinfection
  • Larva currens
  • Malabsorption etc
  • Generally asymptomatic

Treatment: ivermectin

Prevention: hygiene

84
Q

Filariasis

A

A variety of nematode infections spread by blackflies and mosquitoes

Divided according to where the adult worm lives

  • Lymphatic filariasis (Wuchereria, Brugia)
  • Subcutaneous filariasis (Onchocerciasis, Mansonella, Loa loa)
  • Serous cavity filariasis (Mansonella, Dirofilaria)

Adult worms release larvae (microfilariae) taken up by vector

Damage to tissues results either from:

  • Adult worms: lymphatic filariasis (elephantiasis, scrotal swelling), also oncho (nodules)
  • Microfilariae: Onchocerciasis (depigmentation, river blindness)

Diagnosis:

  • Find microfilariae (blood film examination, skin snips)
  • Find antibodies (ELISA, IFAT)
  • Find adults (US – “dance sign”, Loa Loa migration)
85
Q

Myiasis

A
  • Parasitisation of human flesh by fly larvae
  • Very common in some areas
  • Occasionally imported
  • Mainly: Bot (S. america) and Tumbu (Africa)
  • Local damage as the maggot eats necrotic flesh
  • Treatment: removal of larva by asphyxiation or surgery
86
Q

MDRTB

A

Resistance to rifampicin and isoniazid

87
Q

Which 3 countries account for most of the world/s TB

A

India
China
Russia

88
Q

Risk factors for MDR TB in Europe

A
  • Pooled risk for MDRTB 10.2 in previous treated vs never treated
  • 6 national studies in: MDRTB more likely to be foreign born, younger than 65, male and HIV positive
  • Prior TB therapy (OR-7.4)
  • Presence of cavities (OR-2.6)
  • History of imprisonment (OR-2.1) (between 1 and 23 treatment cycles)
  • Recreational drug use (OR-3.0)
  • HIV not associated with resistance (OR-0.3)
89
Q

XDRTB

A

Resistant to isoniazid and rifampin, plus any fluoroquinolone and at least one of three injectable second-line drugs (i.e., amikacin, kanamycin, or capreomycin).

Liv Path (24 decks)

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