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GP ACRRM > Infectious diseases > Flashcards

Infectious diseases Flashcards

1
Q

What is the most commonly reported zoonotic disease in Australia

A

Q fever (Coxiella Burnetii)

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2
Q

Microbiology of Q fever

A

Coxiella burnetii

  • gram negative
  • intracellular bacterium
  • low infectious dose in humans (10-15 organisms)
  • incubation period 2-3 weeks depending on infectious dose
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3
Q

Transmission of Q fever

A

Inhalation of aerosols or dust contaminated with secretions from infected animals (birth products, faeces, urine)
Main source for human infectious are cattle, sheep and goats

Opportunity for infection in farming, veterinary procedures, slaughtering, butchering, zoo keeping, wildlife carers, dog/cat breeders etc.

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4
Q

Distribution of Q fever

A

Present globally EXCEPT in NZ
Highest rates in Australia are in QLD, NSW and SA
More common in males

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5
Q

Clinical features of Q fever

A

Variable
50% asymptomatic
Acute disease usually resolves spontaneously within 2-6 weeks
Possible symptoms:
- fever, headache, myalgia/arthralgia, cough, flu-like illness, weight loss, pneumonia, nausea, jaundice (rare), meningeal signs (rare), maculopapular truncal rash (rare), hepatitis, osteomyelitis

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6
Q

Diagnosis of Q fever

A

Initial investigations: CBE, LFT, CRP, Urinalysis, NPA for viral PCR, CXR if indicated
DO NOT PERFORM A BLOOD CULTURE IF SUSPECT Q FEVER (safety risk in laboratories)

If other diseases excluded, commence treatment while awaiting C burnetii PCR, and serology to C burnetii, leptospira and brucella species

  • *PCR ideally should be performed within 7 days of symptom onset
  • ** Repeat all serologies 7 days later (Acute Q fever will see 4fold increase)
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7
Q

Chronic Q fever presentation

A

Can occur months - years after initial illness (even if initial illness asymptomatic)
Occurs in 1-5% of infected
Most commonly presents as endocarditis or hepatitis
- much higher risk to those with underlying valvular disease

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8
Q

Presentation of post-Q fever fatigue syndrome

A

Affects 10-15% of patients following acute Q fever
Initial infection may be mild
Chronic fatigue-like picture
Alcohol intolerance commonly reported

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9
Q

Management of Q fever

A

Doxycycline 100mg BD for 14 days
(in pregnancy Bactrim BD + folic acid 5mg orally until 32 weeks - discuss with ID physician)
No value in treating non-pregnant patients following spontaneous recovery

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10
Q

Follow up after acute Q fever

A

Consider echo for ?valvular disease

IF patient at risk of chronic infection (e.g. valvular disease, aneurysm, prosthesis, immunosuppression etc.) repeat serology at 3,6, and 12 months
If NOT at risk, repeat serology at 6 and 12 months

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11
Q

Pre-vaccination assessment for Q-fever vaccine

A

Skin test + C. burnetii serology + medical history aimed at identifying possible previous infection
(all 3 must show no evidence of prior infection before vaccination can be performed)

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12
Q

Distribution of leptospirosis

A

Highest incidence in tropical and subtropical areas, especially Oceania

In Australia, most cases in QLD (particularly Cairns/Hinterland regions) and NT

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13
Q

Risk factors for leptospirosis

A

Demographics:

  • male gender
  • young adults

Behaviour:

  • occupational exposure (most significant source in Australia)
  • Dairy/cane/banana farmers
  • Abattoir workers
  • recreational exposure (swimming or rafting in freshwater)
  • International travel and ecotourism in tropics

Environmental drivers:

  • tropical and subtropical climate
  • high rainfall and flooding
  • poor sanitation
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14
Q

How is leptospirosis spread

A

Colonise kidneys of infected mammals - spread into environment via urine where can survive for weeks -> humans infected through direct contact with contaminated soil/water or infected animals

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15
Q

Incubation period of leptospirosis

A

5-14 days (range 2-30 days)

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16
Q

Clinical presentation of leptospirosis

A

BIPHASIC:
Acute/bacteraemic phase
- Sudden onset fever, myalgia, headache
- calf tenderness and conjunctival suffusion [redness without exudate] are characteristic (but not always present)
- nonspecific symptoms (anorexia, nausea, vomiting, abdo pain, dizziness, lethargy, arthralgia, eye pain, photophobia, rash)

Late/Immune phase:

  • > 7 days from symptom onset
  • immunologically mediated organ damage occurs (renal failure, pulmonary haemorrhage, myocarditis, arrhythmias, shock, liver failure, coagulopathy, neurological complications)
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17
Q

What is Weil’s disease

A

Classic triad of severe leptospirosis consisting of:

  • jaundice
  • renal failure
  • haemorrhage
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18
Q

Case definition of confirmed leptospirosis

A

EITHER:
- isolation of pathogenic leptospira species on culture
- fourfold or greater rise in MAT titre obtained at least 2 weeks apart (ideally at same lab)
OR
- a single leptospira MAT titre >400 supported by positive ELISA IgM result

A positive PCR or ELISA IgM are suggestive but not confirmed diagnosis

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19
Q

Lab tests for suspected leptospirosis

A

ALWAYS include travel history on request form so correct serovars will be tested

ACUTE PHASE: Collect blood for PCR and IgM ELISA before commencing antibiotics

LATE PHASE: order both IgM ELISA and MAT tests with repeat sample 14 days later

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20
Q

Management of leptospirosis

A

Commence treatment if suspected disease based on risk factors and recent exposure

All for 7 days or as otherwise indicated if longer therapy needed:
Mild disease: PO doxycycline 100mg BD for 7 days

Severe disease:
- IV Benzylpenicillin 1.2g 6 hourly for 7 days
OR
- IV ceftriaxone 1g daily for 7 days

*Jarish-herxheimer reaction can occur within 48 hours of commencing treatment

Plus/minus supportive therapy as indicated
Antibiotics not required if diagnosed AFTER clinical recovery in self-limiting illness

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21
Q

Where in Australia is a diagnosis of Brucellosis most common?

A

Queensland. (80% of Australian cases are diagnosed in QLD)

only approx 30 cases per year in Aus

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22
Q

Risk factors for Brucellosis in Australians

A

Most significant:

  • Feral pig hunting
  • travel to/from and/or consumption of unpasteurised dairy products manufactured in countries with endemic brucella (mediterranean, Middle East, central Asia, India, Central and South America, Mexico)

Less commonly:

  • farmers, abbatoir workers, animal handlers who have worked in above countries
  • lab workers handling brucella cultures
  • people involved in transport/processing of feral pig carcasses
  • vets, dog breeders, household contact of feral pig hunters
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23
Q

Fatality rate of brucellosis

A

2%

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24
Q

Countries where brucella is present in livestock

A 
Mediterranean countries (Portugal, Spain, southern France, Italy, Greece, Turkey)
Middle East
Central Asia
India
Central and South America
Mexico
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25
Q

How is brucellosis infection contracted

A

B. suis (Australia) direct contact with feral pig tissue/body fluids via skin abrasions and mucous membranes (can also be transmitted from infected farm/pig dogs)
B. melitensis/B. abortus: ingestion of unpasteurised dairy products (especially cheese) or direct contact with animal tissues/body fluids

Aerosol transmission possible in lab environments handling brucella cultures

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26
Q

Phases of brucellosis

A

Incubation phase: usually 2-4 weeks (range 5 days - 5 months)
Acute phase: symptoms commence
Chronic phase

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27
Q

Common symptoms of brucellosis

A

usually a GRADUAL onset

Fever (relapsing, mild or protracted)
Sweats
Anorexia +/- weight loss
Fatigue
Malaise
Arthralgia, myalgia, back pain
Headache
Depression (often severe relative to other symptoms)
Epididymo-orchitis
?spontaneous 1st or 2nd trimester miscarriage
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28
Q

Complications of brucellosis

A
  • Osteoarticular disease (particularly sacroiliitis)
  • Hepatosplenic brucellomas (chronic suppurative granulomatous process)
  • neurobrucellosis (presents as acute or chornic lymphocytic meningitis)
  • Cardiovascular manifestations (main cause of death) including endocarditis, aneurysms, myocarditis, pericarditis
  • Respiratory complications (bronchopneumonia, pleural adhesions)
  • endophthalmitis
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29
Q

Diagnosing brucellosis

A

In acute infection:
- Serum IgM often detectable but can be a cross reaction with other infections
- confirmed with brucella IgG or 4fold increase in titres
OR
with blood culture (make sure to notify lab if suspected as is a biohazard)

Relapsing infection:

  • blood culture
  • typical granulomatous histopath of involved tissue
  • PCR of involved tissue
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30
Q

Management of brucellosis

A

Dual therapy with:
Oral doxycycline 100mg BD for 6 weeks
PLUS
7 days of IV gentamicin (5mg/kg)

(rifampicin 600mg daily for 6 weeks if gentamicin contraindicated)

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31
Q

Transmission route of toxoplasmosis

A

Faecal-oral route

  • ingestion of undercooked contaminated meat (pork, lamb, venison) or shellfish
  • accidental ingestion through contact with contaminated cat faeces (cleaning litter box, contaminated soil etc. )

Vertical transmission
Organ transplant/blood transfusion (rare)

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32
Q

Pathogen responsible for toxoplasmosis

A

Parasite toxoplasma gondii

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33
Q

Risks of negative outcomes of toxoplasmosis in pregnacy

A

1st trimester:

  • low risk of vertical transmission (approx 10%)
  • high risk of abnormalities (up to 80%)

2nd trimester:

  • moderate risk of vertical transmission (approx 30%)
  • Low risk of abnormalities (approx 20%)

3rd trimester:

  • high risk of vertical transmission (up to 80%, higher risk at higher gestation)
  • low risk of abnormalities (<10%)
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34
Q

Congenital abnormalities in congenital toxoplasmosis (9)

A
  • Chorioretinitis/retinal scarring
  • hydrocephalus
  • intracranial calcification
  • hepatosplenomegaly
  • pneumonia
  • thrombocytopaenia
  • lymphadenopathy
  • myocarditis
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35
Q

Clinical features of toxoplasmosis

A 
Most patients will be completely asymptomatic
Mild illness may have:
- flu-like illness
- malaise
- myalgia
s
- swollen lymph glands

Severe disease (most likely in immunocompromised)

  • ocular toxoplasmosis (blurred vision, photophobia, ocular pain, red eye or tearing
  • “brain damage”
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36
Q

Diagnosing toxoplasmosis

A

Consider testing in pregnant women with symptoms of acute toxoplasmosis

IgG and IgM initially - if both positive POSSIBLE recent infection (IgM can be positive for years)

Repeat serology for IgM, IgA and/or IgG titre and avidity
- IgA, rising IgG and/or low IgG avidity are more specific for recent infection

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37
Q

Management of toxoplasmosis in pregnancy

A

USS to detect abnormalities
Amniocentesis for PCR and/or culture
(if both above are negative consider pharmacological treatment with spiramycin, (or atovaquone or azithromycin if >12 weeks))
Counsel re: termination if amniocentesis PCR positive/abnormal ultrasound

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38
Q

Congenital toxoplasmosis management in neonate

A 
Paediatrician at birth
Ophthalmological assessment
Cerebral ultrasound
Whole blood at birth for PCR, serology for specific IgM and/or IgA, persistent IgG
CSF for PCR

Spiramycin oral syrup for first 12 months with regular paeds or ID review

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39
Q

Pathogen responsible for tuberculosis

A

Most commonly Mycobacterium tuberculosis

Can also be caused by closely related species such as M. africanum and M. bovis

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40
Q

Global epidemiology of tuberculosis

A

> 1/3 of world population is infected with TB

Absolute number has been falling since 2006

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41
Q

Countries with highest number of tuberculosis incident cases

A 
India (26% of cases worldwide)
China (12% of cases worldwide)
South Africa
Indonesia
Pakistan
42
Q

Risk of latent TB developing into active TB

A

10% risk in lifetime - greatest risk in first 2y of infection

43
Q

Populations at higher risk of TB exposure (6)

A

Elderly patients
Aboriginal Australians
Torres Strait Island residents (exposure to PNG where incidence is high)
Migrants/refugees from high burden countreis (esp. Sub-saharan Africa, India, China, other Asian countries)
Healthcare workers in high burden countries
Homelessness/shelter-dwelling/incarceration (more so overseas/US)

44
Q

People at highest risk of acquiring ACTIVE TB (15)

A 
HIV infection
IV drug use
Alcoholism
Diabetes (3x increased risk)
Silicosis
Immunosuppressive therapy
Therapy with TNF-alpha antagonists
Head and neck cancer
Haematological malignancies
End-stage renal disease
Intestinal bypass surgery or gastretctomy
Chronic malabsorption syndromes
Low body weight
Smoking (2x increased risk)
Age <5y
45
Q

Risk factors for extrapulmonary TB

A

Childhood
HIV infection
Immunocompromised state

46
Q

Microbiology of TB

A

(M. tuberculosis)
Slow-growing obligate aerobe
Facultative intracellular parasite
Acid-fast bacillus

Able to survive ingestion by phagocytes and then proliferate within them, allowing invastion of local lymph nodes and spread to extrapulmonary sites

47
Q

Transmission routes of TB

A

Airborne aerosol - primary mode of spread, from someone in infectious stage
- pulmonary TB is most infectious form

Transdermal and GI transmission has been reported

Children <10y are usually considered non-infectious

48
Q

Factors which increase risk of TB transmission

A

Crowded living or closed environments (e.g. submarines, transcontinental flights etc. )

Approx 20% of household contacts will develop infection

49
Q

Classic presentation of active pulmonary TB

A 
Cough
Weight loss/anorexia
Fever
Night sweats
Haemoptysis
Chest pain
Fatigue
(May present as non-resolving pneumonitis in elderly)

Abnormal breath sounds esp over upper lobes
Rales or bronchial breathing

50
Q

Non-specific signs and symptoms of extrapulmonary TB

A

Leukocytosis
Anaemia
Hyponatraemia (ADH-like hormone release from affected lung tissue)
Lymphadenopathy (painless, bilaterally, typically anterior and posterior cervical chain, or supraclavicular LN)

51
Q

Potential signs and symptoms of tuberculous meningitis

A

Headache (intermittent or persistent ) for 2-3 weeks
Mental status changes (from subtle - confusion - coma)
Neurological deficit
Low-grade fever (may be absent)

52
Q

What is Pott disease

A

Skeletal tuberculosis disease occurring in the spine

53
Q

Signs and symptoms of skeletal tuberculosis

A

Most commonly occur in spine:

  • back pain/stiffness
  • lower extremity paralysis in 50% of patients

Tuberculous arthritis

  • usually monoarticular
  • knees and hips most commonly (followed by ankle, elbow, wrist and shoulder)
  • pain can precede radiographic changes by weeks-months
54
Q

Signs and symptoms of genitourinary TB

A

Flank pain
Dysuria
Frequent urination

In men:

  • painful scrotal mass
  • prostatitis
  • orchitis
  • epididymitis

In women:

  • can mimic pelvic inflammatory disease
  • sterility (10% of sterility cases worldwide in women secondary to TB, 1% in developed countries)
55
Q

Signs and symptoms of Gastrointestinal TB

A

Depends on site of infection

  • nonhealing ulcers of mouth or anus
  • difficulty swallowing (oesophageal disease)
  • abdominal pain mimicking PUD (stomach or duodenal disease)
  • malabsorption (small intestine)
  • pain, diarrhoea or haematochezia (colonic disease)
56
Q

Investigations to order in suspected active TB

A

CXR (ensure to clearly note suspicion on order request)
Sputum MCS(3x early morning specimens on 3 separate days)
- Ziehl Neelsen stain, if positive then cultures of molecular assays to confirm if MTB complex present

57
Q

Typical CXR findings in primary TB

A

Children: anywhere in lung fields
Adults: predilection for upper or lower zone

Features:

  • consolidation (patchy to lobar)
  • tuberculoma (caseating granuloma)
  • Ghon lesion (calcified tuberculoma)
  • Ghon Complex
  • Ranke Complex

Ipsilateral hilar and contiguous mediastinal LN very common in children

Cavitation uncommon at this stage (<30%)

58
Q

What is a Ghon lesion

A

A calcified caseating granuloma seen in tuberculosis

59
Q

What is a Ghon complex

A

A Ghon lesion (calcified tuberculoma) + ipsilateral lymph node

60
Q

What is a Ranke Complex

A

A Ghon lesion + calcified node

61
Q

Typical CXR findings in secondary/reactivated TB

A

Strong predilection for upper zones

  • patchy consolidation
  • cavitating lesion in upper lobes
  • hilar nodal enlargement much less common than in primary disease (30%)
  • tuberculomas rare at this stage
62
Q

Typical CXR findings of miliary TB

A

1-3mm diameter nodules uniform in size and distribution throughout both lungs

63
Q

Investigating for latent TB

A

Tuberculin skin test (Mantoux test)
- false positives in BCG vaccination history and exposure to environmental mycobacterium spp.

Interferon gamma release assay:

  • unaffected by previous BCG vaccination
  • medicare rebate only if patient immunosuppressed (OOP cost up to $100)
  • not suitable children <2y
  • cannot diagnose active TB (can be negative in active disease)
64
Q

Management of active tuberculosis

A

Refer to hospital-based infectious disease or respiratory service for inpatient commencement of treatment (given risk of transmission)

1. Isoniazid daily for 6 months
PLUS
2. Rifampicin daily for 6 months
PLUS
3. Ethambutol daily for 2 months
PLUS
4. Pyrazinamide daily for 2 months
65
Q

Management of latent TB

A

MAY be suitable for GP management if <35y with normal LFTs, otherwise refer to ID/respiratory

Ensure to exclude active disease based on CXR and symptoms first

Isoniazid daily for 6-9 months

66
Q

Epidemiology of latent TB in Australians

A

Occurs in approx 5% of Australian residents (17% of overseas-born Australians, 0.4% of Australian-born residents)

Recommended that all refugees are screened preferable within 1 month of arrival

67
Q

Side effects of isoniazid

A

Hepatotoxicity (higher risk if pre-therapy LFT derangement or age >50y)
GI upset
Acne
Peripheral neuropathy

68
Q

What is enterobiasis

A

Infestation of threadworm (AKA pinworms) helminth.

69
Q

Epidemiology of threadworm

A

Most common intestinal worm in Australia
More common in children (prevalence 10-50%)
Infection usually asymptomatic

70
Q

Microbiology of threadworm

A

Enterobius vermicularis

  • lifespan 11-35 days (chronic disease due to reinfection)
  • humans are only reservoir
  • direct transmission of eggs from anus to mouth from same or different person, hatch to larvae in small bowel, mature in colon, females migrate outside anus nocturnally and lay eggs in perianal folds.
  • 2-13mm in size, yellowish-white colour
71
Q

Clinical presentation of threadworm

A

Asymptomatic in the majority
Perianal itch or prickling pain (usually nocturnal or early morning due to nocturnal activity of female worm)
Restless sleep or difficulty sleeping in child
Abdominal discomfort and anorexia is rare
Vaginal itching can also occur

72
Q

Management of threadworm

A

OTC: Combantrim (either mebendazole 100mg (50mg if <10kg) single dose OR pyrantel 10mg/kg up to 1g single dose)
OR
Prescription: Albendazole 400mg (200mg if <10kg) single dose

Consider treating all household contacts and retreatment in 2 weeks in case of reinfection
Advise re: hygiene measures

73
Q

Prevention of threadworm

A

Effective handwashing (especially before handling food)
Short nails
Discouraging scratching of bare anal area
Discouraging nail biting
Bathing or showering daily
Clean underwear, nightclothes and bedsheets frequently with hot water

74
Q

Risk factors for giardiasis

A

Children who are not toilet trained
Healthcare and childcare workers
International travelers (from or to developing areas)
Hikers and campers

75
Q

Microbiology of giardiasis

A

Giardia intestinalis (AKA duodenalis OR lamblia)

Flagellated bi-nucleated protozoan

Highly infectious cysts (infectious dose = 10)
-> trophozoites which multiply and colonise small intestine and adhere to brush border of enterocytes to cause malabsorption

Incubation period 7-10 days

Protective outer shell makes tolerant to chlorine and survival outside of host for long periods of time

76
Q

Clinical presentation of giardia

A

Most often asymptomatic

If symptoms present:

  • foul smelling greasy or watery diarrhoea
  • abdominal cramps
  • fatigue
  • bloating
  • anorexia
77
Q

Management of giardiasis

A

Treatment of asymptomatic immunocompetent carriers usually unnecessary

If symptomatic:
1. Tinidazole 2g single dose
OR
2. Metronidazole 2g daily for 3 days
OR
2. Metronidazole 400mg 8 hourly or 5 days (preferred regime in pregnancy)
78
Q

Epideimology of roundworm

A

Most common worldwide parasitic worm infestation
Prevalence and intensity of infection highest in children 3-8yo
RARELY acquired in Australia

transmission only from contaminated soil, not from fresh faeces or direct human-to-human

79
Q

Microbiology of roundworm

A

Ascaris lumbircoides
- large intestinal roundworm (up to 30cm long)
- eggs can remain viable for years
- eggs take minimum 18 days to mature to infective form of eggs
Incubation period 4-8 weeks

80
Q

Life cycle of roundworm

A

Mature (infective) eggs ingestion from contaminated hands/soil/foods

  • > larvae hatch and invade intestinal mucosa
  • > carried via circulation to lungs
  • > mature in lungs for 10-14 days
  • > larvae ascend bronchial tree to throat and are swallowed
  • > adult worms develop in intestine and lay up to 200,000 eggs per day

Life cycle takes 4-8 weeks
Adult worms can live for 1-2 years

81
Q

Clinical presentation of roundworm

A

Often asymptomatic

  • live worms in stool/mouth/anus/nose
  • vague to severe abdominal pain
  • nausea/vomiting +/- worms in vomitus
  • diarrhoea +/- bloody stools +/- worms
  • fatigue, weight loss
  • nutritional deficiencies and failure to thrive in children with heavy infestation
  • pancreatic, biliary or bowel obstruction are possible

Pulmonary symptoms due to larval migration are possible:

  • wheeze
  • cough
  • fever
  • eosinophilia
  • pulmonary infiltration
82
Q

Management of round worm

A
  1. Albendazole 400mg single dose (non-PBS prescription)
    OR
  2. Mebendazole 100mg BD for 3 days (i.e. combantrim, note longer and higher dose course than for tapeworm)
    OR
  3. Pyrantel 10mg/kg up to 1g single dose +/- repeat in 7 days
83
Q

Hookworm in Australia

A

Rare in general
- majority of cases in remote Indigenous communities and in migrants from endemic countries
More common in tropical regions

84
Q

Lifecycle of hookworm

A
  1. eggs in faeces contaminate soil
  2. Rhabditiform larva hatch and develop into filariform larva in the environment
  3. Filariform larva penetrate skin, enter circulation and exit into the lungs by penetrating through alveolar walls
  4. Larvae migrate up the bronchial tree to pharynx and are swallows
  5. Develop into adult worms in the distal jejenum where they attach to the intestinal wall and begin reproducing
85
Q

Parasites that cause intestinal hookworm

A

Ancylosoma duodenale (only relevant one in Australia)

Necator americanus

Ancylostoma caninum (from dogs, cannot reproduce in humans but can cause an eosinophilic enteritis)

86
Q

Clinical presentation of hookworms

A

Most will be asymptomatic

Possible symptoms: diarrhoea, rash, abdominal pains

Possible complications:

  • iron deficiency +/- anaemia
  • failure to thrive ( in children with severe infestatiosn)
87
Q

Management of hookworm

A
  1. Albendazole 400mg single dose (PBS listed)
    OR
  2. mebendazole 100mg BD for 3 days (longer and higher frequency course than for tapeworm)
    OR
  3. Pyrantel 10mg/kg daily for 3 days (note longer course than tapeworm or roundworm)

+/- iron supplementation etc. as indicated

88
Q

Transmission of HBV

A

*Vertical (common in countries without infant vaccination)
(breastfeeding does NOT increase risk of transmission)
*Horizontal - household sharing of toothbrushes, razors, nail files etc
*Sexual - unprotected vaginal, anal or oral sex
*Percutaneous - re-used injecting equipment, tattooing, body piercing, acupuncture
*Medically acquired - blood transfusion or organ transplants (overseas), dentistry, surgery, dialysis, needlestick injuries, body fluid contact to HCW

89
Q

Natural history of acute hepatitis B infection

A
  1. Incubation (4-12 weeks)
  2. Symptomatic hepatitis (4-12 weeks)
    - fever, fatigue, anorexia, nausea, dark urine, jaundice, myalgia, RUQ pain (kids often asymptomatic)
  3. Recovery period - ALT levels normalise
  4. Clearance phase - HBsAg clears from serum after few months, coinciding with development of anti HBs

If HBsAg persists for 6 months, indicates progression to Chronic Hep B

90
Q

Phases of chronic Hepatitis B infection

A

Immune tolerance:

  • HBeAg positive, high HBV DNA (>20,000), normal ALT
  • can persist for decades
  • low risk of progression to advanced liver disease

Immune clearance:

  • Active, immune-mediated cytotoxic response to infected liver cells (liver injury from HBV is caused by the immune response TO the virus)
  • Fluctuating HBV DNA and ALT levels. Positive HBeAg
  • at risk of progression to cirrhosis or HCC therefore should consider for treatment

Immune Control:

  • HBV low/undetectable (<2000), normal LFTs, Anti HbE positive
  • liver inflammation minimal, do not require treatment unless there is advanced liver disease

Immune Escape:

  • Negative HBeAg, Positive Anti-HBe, detectable HBV DNA (>2000)
  • can reach this phase from immune control state or progress directly from HBeAg positive chronic hepatitis to negative
  • at risk of progression to cirrhosis and HCC therefore should be considered for treatment
91
Q

In which phases should chronic hepatitis B patients be considered for treatment

A

Immune control phase (fluctuating HBV DNA and ALT levels, positive HBeAg)
OR
Immune escape phase
Negative HBeAg, positive anti-HBe, detectable viral load (HBV DNA >2000)

(entecavir, tenofovir, PEG-interferon)

92
Q

Who to test for hepatitis B

A
  • ATSI people
  • people born in intermediate and high prevalence countries
  • pregnant women
  • adults at increased risk of transmission (sexual or household contacts, MSM, PWID, people with multiple sexual partners, haemodialysis patients)
  • Hep C or HIV patients
  • Pre-chemotherapy or immunosuppressive therapy
  • people with clinical presentation of liver disease or raised ALT +/- AFP of unknown aetiology
  • HCW at risk of needle-stick injuries
  • members of armed forces
93
Q

Initial assessment of patients with chronic hepatitis B

A
  • risk factors for acquisition of HBV
  • risk factors for severe disease (age, alcohol, smoking, co-infection)

Investigations:

  • HBV DNA (viral load)
  • HAV, HCV, HDV serology
  • HIV serology
  • HbeAg and anti-HBe to confirm phase of infection
  • LFTs
  • CBD
  • coagulation studies (INR, PT) assess synthetic function
  • AFP ?HCC
94
Q

Determining acute v chronic hepatitis on serology

A

(usually likely to determine via symptoms but serology to confirm)
Both have positive HBsAg, Anti-HBc, and negative Anti-HbS.
If suspect acute HBV infection/recent exposure, request IgM anti-HbC which is ONLY positive in acute disease

95
Q

Monitoring of Chronic HBV (frequency and investigations)

A

Immune tolerance phase:

  • 6-12 monthly LFT, HBeAg/anti-HBe
  • 12 monthly HBV DNA

Immune control phase:
- 6-12 montly LFT, yearly HBV DNA

Immune clearance or escape: consider treatment

On treatment: according to treatment regimen

Those at risk of HCC (Asian males >40y, Asian females >50y, Africans >20y, all patients with cirrhosis, patients with family history of HCC):
6 monthly USS and AFP, if abnormal for 4-phase CT or contrast MRI

96
Q

High risk factors for HCC in patients with HBV

A 
Asian Males >40y
Asian females >50y
Africans >20y
All patients with cirrhosis
Patients with a family history of HCC

(6 monthly USS and AFP)

97
Q

Prevention of HBV

A

Vaccination

  • pre-vax testing recommended for all from high-risk groups
  • post-vax testing required for high-risk groups also (approx 5% will not acquire immunity)
  • 3 dose regime over 6 months
98
Q

Management of non-response to full course of HBV vacccination

A

EITHER fourth double dose
OR
further 3 doses at monthly intervals

Further testing at least 4 weeks after final dose

99
Q

When to refer patients with HBV

A

Severe acute exacerbation (or acute HBV infection)

  • potential for fulminant disease
  • reactivation during ISS or chemotherapy (urgent anti-viral therapy needed
  • Cirrhosis (especially if decompensated)
  • Possible HCC found on surveillance
100
Q

HBV in pregnancy

A

Risk of vertical transmission is 95% without intervention and 5% with intervention

All infants should receive HBIG and first dose of HBV vaccine within 12 hours of birth then 3 doses within the first 6-12 months of life

Newborn should be tested for HBsAg and anti-HBs at least 3 months after final dose

Mothers with flare or high viral load have higher risk of transmission and should be counselled about potential antiviral therapy
antiviral therapy does put potential risks to foetal development

GP ACRRM (14 decks)

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