Infectious diseases Flashcards
What is the most commonly reported zoonotic disease in Australia
Q fever (Coxiella Burnetii)
Microbiology of Q fever
Coxiella burnetii
- gram negative
- intracellular bacterium
- low infectious dose in humans (10-15 organisms)
- incubation period 2-3 weeks depending on infectious dose
Transmission of Q fever
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.
Distribution of Q fever
Present globally EXCEPT in NZ
Highest rates in Australia are in QLD, NSW and SA
More common in males
Clinical features of Q fever
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
Diagnosis of Q fever
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)
Chronic Q fever presentation
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
Presentation of post-Q fever fatigue syndrome
Affects 10-15% of patients following acute Q fever
Initial infection may be mild
Chronic fatigue-like picture
Alcohol intolerance commonly reported
Management of Q fever
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
Follow up after acute Q fever
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
Pre-vaccination assessment for Q-fever vaccine
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)
Distribution of leptospirosis
Highest incidence in tropical and subtropical areas, especially Oceania
In Australia, most cases in QLD (particularly Cairns/Hinterland regions) and NT
Risk factors for leptospirosis
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
How is leptospirosis spread
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
Incubation period of leptospirosis
5-14 days (range 2-30 days)
Clinical presentation of leptospirosis
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)
What is Weil’s disease
Classic triad of severe leptospirosis consisting of:
- jaundice
- renal failure
- haemorrhage
Case definition of confirmed leptospirosis
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
Lab tests for suspected leptospirosis
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
Management of leptospirosis
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
Where in Australia is a diagnosis of Brucellosis most common?
Queensland. (80% of Australian cases are diagnosed in QLD)
only approx 30 cases per year in Aus
Risk factors for Brucellosis in Australians
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
Fatality rate of brucellosis
2%
Countries where brucella is present in livestock
Mediterranean countries (Portugal, Spain, southern France, Italy, Greece, Turkey) Middle East Central Asia India Central and South America Mexico
How is brucellosis infection contracted
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
Phases of brucellosis
Incubation phase: usually 2-4 weeks (range 5 days - 5 months)
Acute phase: symptoms commence
Chronic phase
Common symptoms of brucellosis
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
Complications of brucellosis
- 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
Diagnosing brucellosis
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
Management of brucellosis
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)
Transmission route of toxoplasmosis
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)
Pathogen responsible for toxoplasmosis
Parasite toxoplasma gondii
Risks of negative outcomes of toxoplasmosis in pregnacy
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%)
Congenital abnormalities in congenital toxoplasmosis (9)
- Chorioretinitis/retinal scarring
- hydrocephalus
- intracranial calcification
- hepatosplenomegaly
- pneumonia
- thrombocytopaenia
- lymphadenopathy
- myocarditis
Clinical features of toxoplasmosis
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”
Diagnosing toxoplasmosis
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
Management of toxoplasmosis in pregnancy
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
Congenital toxoplasmosis management in neonate
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
Pathogen responsible for tuberculosis
Most commonly Mycobacterium tuberculosis
Can also be caused by closely related species such as M. africanum and M. bovis
Global epidemiology of tuberculosis
> 1/3 of world population is infected with TB
Absolute number has been falling since 2006
Countries with highest number of tuberculosis incident cases
India (26% of cases worldwide) China (12% of cases worldwide) South Africa Indonesia Pakistan
Risk of latent TB developing into active TB
10% risk in lifetime - greatest risk in first 2y of infection
Populations at higher risk of TB exposure (6)
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)
People at highest risk of acquiring ACTIVE TB (15)
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
Risk factors for extrapulmonary TB
Childhood
HIV infection
Immunocompromised state
Microbiology of TB
(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
Transmission routes of TB
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
Factors which increase risk of TB transmission
Crowded living or closed environments (e.g. submarines, transcontinental flights etc. )
Approx 20% of household contacts will develop infection
Classic presentation of active pulmonary TB
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
Non-specific signs and symptoms of extrapulmonary TB
Leukocytosis
Anaemia
Hyponatraemia (ADH-like hormone release from affected lung tissue)
Lymphadenopathy (painless, bilaterally, typically anterior and posterior cervical chain, or supraclavicular LN)
Potential signs and symptoms of tuberculous meningitis
Headache (intermittent or persistent ) for 2-3 weeks
Mental status changes (from subtle - confusion - coma)
Neurological deficit
Low-grade fever (may be absent)
What is Pott disease
Skeletal tuberculosis disease occurring in the spine
Signs and symptoms of skeletal tuberculosis
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
Signs and symptoms of genitourinary TB
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)
Signs and symptoms of Gastrointestinal TB
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)
Investigations to order in suspected active TB
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
Typical CXR findings in primary TB
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%)
What is a Ghon lesion
A calcified caseating granuloma seen in tuberculosis
What is a Ghon complex
A Ghon lesion (calcified tuberculoma) + ipsilateral lymph node
What is a Ranke Complex
A Ghon lesion + calcified node
Typical CXR findings in secondary/reactivated TB
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
Typical CXR findings of miliary TB
1-3mm diameter nodules uniform in size and distribution throughout both lungs
Investigating for latent TB
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)
Management of active tuberculosis
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
Management of latent TB
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
Epidemiology of latent TB in Australians
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
Side effects of isoniazid
Hepatotoxicity (higher risk if pre-therapy LFT derangement or age >50y)
GI upset
Acne
Peripheral neuropathy
What is enterobiasis
Infestation of threadworm (AKA pinworms) helminth.
Epidemiology of threadworm
Most common intestinal worm in Australia
More common in children (prevalence 10-50%)
Infection usually asymptomatic
Microbiology of threadworm
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
Clinical presentation of threadworm
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
Management of threadworm
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
Prevention of threadworm
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
Risk factors for giardiasis
Children who are not toilet trained
Healthcare and childcare workers
International travelers (from or to developing areas)
Hikers and campers
Microbiology of giardiasis
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
Clinical presentation of giardia
Most often asymptomatic
If symptoms present:
- foul smelling greasy or watery diarrhoea
- abdominal cramps
- fatigue
- bloating
- anorexia
Management of giardiasis
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)
Epideimology of roundworm
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
Microbiology of roundworm
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
Life cycle of roundworm
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
Clinical presentation of roundworm
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
Management of round worm
- Albendazole 400mg single dose (non-PBS prescription)
OR - Mebendazole 100mg BD for 3 days (i.e. combantrim, note longer and higher dose course than for tapeworm)
OR - Pyrantel 10mg/kg up to 1g single dose +/- repeat in 7 days
Hookworm in Australia
Rare in general
- majority of cases in remote Indigenous communities and in migrants from endemic countries
More common in tropical regions
Lifecycle of hookworm
- eggs in faeces contaminate soil
- Rhabditiform larva hatch and develop into filariform larva in the environment
- Filariform larva penetrate skin, enter circulation and exit into the lungs by penetrating through alveolar walls
- Larvae migrate up the bronchial tree to pharynx and are swallows
- Develop into adult worms in the distal jejenum where they attach to the intestinal wall and begin reproducing
Parasites that cause intestinal hookworm
Ancylosoma duodenale (only relevant one in Australia)
Necator americanus
Ancylostoma caninum (from dogs, cannot reproduce in humans but can cause an eosinophilic enteritis)
Clinical presentation of hookworms
Most will be asymptomatic
Possible symptoms: diarrhoea, rash, abdominal pains
Possible complications:
- iron deficiency +/- anaemia
- failure to thrive ( in children with severe infestatiosn)
Management of hookworm
- Albendazole 400mg single dose (PBS listed)
OR - mebendazole 100mg BD for 3 days (longer and higher frequency course than for tapeworm)
OR - Pyrantel 10mg/kg daily for 3 days (note longer course than tapeworm or roundworm)
+/- iron supplementation etc. as indicated
Transmission of HBV
*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
Natural history of acute hepatitis B infection
- Incubation (4-12 weeks)
- Symptomatic hepatitis (4-12 weeks)
- fever, fatigue, anorexia, nausea, dark urine, jaundice, myalgia, RUQ pain (kids often asymptomatic) - Recovery period - ALT levels normalise
- 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
Phases of chronic Hepatitis B infection
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
In which phases should chronic hepatitis B patients be considered for treatment
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)
Who to test for hepatitis B
- 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
Initial assessment of patients with chronic hepatitis B
- 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
Determining acute v chronic hepatitis on serology
(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
Monitoring of Chronic HBV (frequency and investigations)
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
High risk factors for HCC in patients with HBV
Asian Males >40y Asian females >50y Africans >20y All patients with cirrhosis Patients with a family history of HCC
(6 monthly USS and AFP)
Prevention of HBV
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
Management of non-response to full course of HBV vacccination
EITHER fourth double dose
OR
further 3 doses at monthly intervals
Further testing at least 4 weeks after final dose
When to refer patients with HBV
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
HBV in pregnancy
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
