Infection control guidelines – Pacific Nations

PPHSN Infection Prevention and  Control Guidelines –  2010 

These are likely to be updated before too long.  They are produced by PICNet – Pacific regional Infection Control Network.

Updated PNG Infection Control Guidelines are expected soon.

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Hepatitis E- more important issues for Pacific nations

Please see this previously posted presentation from Prof. Josh Davis about HEV– an excellent overview – tells the Australian part of the story – endemicity in pigs (genotype 3) and local foodborne outbreaks.

The only survey of seroprevalence in the Pacific was published in 2014, referencing data acquired from Kiribati, PNG and Fiji 2003-5 – essential reading.  Overall 15% seroprevalence in PNG, higher in the highlands.  It references some data showing that genotype 3 has been found in pigs in New Caledonia.

Rapid testing reference referred today by Joe is here – an Italian study – almost all cases were genotype 1 which may make the tests less reliable in PNG.  Another good paper for your journal club.

As discussed, there will be an unknown morbidity occurring in PNG, especially in pregnant women and it is almost certain that a large zoonotic reservoir exists. Ripe for some proper research and important that local testing is established. 

According to WHO, a recombinant effective vaccine to prevent hepatitis E virus infection has been developed and is licensed in China, but is not yet available elsewhere.

PNG should coloured red! 

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“UTI” – Requiem for a Heavyweight – a landmark paper

A really important paper to consider closely – i will send on a PDF via email as general access not available.  This editorial from the BMJ is a worthwhile read as well.

AIMED - Let's talk about antibiotics

A recent paper, “Urinary Tract Infection”-Requiem for a Heavyweight  by Dr Thomas Finucaine skillfully unpacks many key issues, coupling this with a consideration of the emerging knowledge of the urinary microbiome and virome, suggesting that the term “UTI” might better be referred to as a “urinary dysbiosis”.  The paper is worth a detailed read – here is the start of the abstract –

“Urinary tract infection” (“UTI”) is an ambiguous, expansive, overused diagnosis that can lead to marked, harmful antibiotic overtreatment. “Significant bacteriuria,” central to most definitions of “UTI,” has little significance in identifying individuals who will benefit from treatment. “Urinary symptoms” are similarly uninformative. Neither criterion is well defined. Bacteriuria and symptoms remit and recur spontaneously. Treatment is standard for acute uncomplicated cystitis and common for asymptomatic bacteriuria, but definite benefits are few. Treatment for “UTI” in older adults with delirium and bacteriuria is widespread but no evidence supports…

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You are what you eat – or should our gut microbiome be considered an important body system in its own right?

AIMED - Let's talk about antibiotics

Guest posting: Assoc. Prof. Josh Davis,  Principal Research Fellow/NHMRC Career Development Fellow, Menzies School of Health Research, Senior Staff Specialist Infectious Diseases Physician, John Hunter Hospital, Conjoint Professor School of Medicine and Public Health, University of Newcastle

The diverse bacterial communities which live in our gastrointestinal tract (primary in the colon), are collectively known as the “gut microbiota” and their collective genes are termed the “microbiome“.  A majority of the bacterial species cannot cultivated and require direct molecular techniques to ennumerate them.  Consideration of the microbiome is extremely topical in many fields of health-related research. At the recent major annual meeting of the American Society for Microbiology (ASM Microbe), the gut microbiome had its own stream (no pun intended – and the colour coding wasn’t brown) within the conference program, containing scores of research presentations in this field. In fact, one conference delegate, science writer and microbiologist Ed Yong, insisted…

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Neisseria gonnorhoeae – brief review and data on AMR in PNG

A brief Neisseria gonorrhoeae update from our registrar Ian Marr at our regular bug of the week teaching round. We still culture it regularly from our samples – susceptibility testing is done at a reference laboratory. PCR diagnosis from early pass urine is the mainstay for most patients (main test method for C. trachomatis as well.

Please seek out this reference – here is the full text link.  Abstract below.   Good for a journal club.  I’ve not found anything more recent. Perhaps someone can check with PNGIMR and with Dr Valleley.  

P N G Med J. 2010 Mar-Jun;53(1-2):15-20.  Neisseria gonorrhoeae isolates from four centres in Papua New Guinea remain susceptible to amoxycillin-clavulanate therapy.  Toliman PJ1, Lupiwa T, Law GJ, Reeder JC, Siba PM.

Antibiotic-resistant strains of Neisseria gonorrhoeae have the potential to undermine treatment and control of gonorrhoea, which remains a highly prevalent sexually transmitted infection (STI) in Papua New Guinea (PNG). The standard treatment regimen for gonorrhoea in PNG based on amoxycillin and clavulanic acid (amoxycillin-clavulanate) was introduced about 15 years ago and there is some concern that over time circulating strains may have developed resistance to this therapy. To investigate this, N. gonorrhoeae isolates (n = 52) were collected from STI clinics in geographically representative centres in PNG and tested for their in vitro susceptibility to a range of antibiotics. All 52 isolates tested were found susceptible to amoxycillin-clavulanate, despite 40% (n = 21) being penicillinase producers and thus resistant to penicillin. These findings indicate that amoxycillin-clavulanate therapy remains an effective treatment for gonococcal infections in PNG, and support the maintenance of the present standard treatment for gonorrhoea in PNG.

Reference

  • WHO STD Laboratory Reference Manual – this is a good reference to go to for advice on key techniques – it is essential that we get a reliable culture system working again in PMGH for instance and this is a good starting point.
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WHO Core Components for Infection Control

Essential guidelines published last year by the WHO.  There is an excellent brief (2 minute) video review of the components. This is the single page info graphic:

Remember also to complete the 10 free Australian Commission on Safety and Quality in Healthcare short online learning modules for Infection Prevention and Control. Enroll here!

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Q fever and other rickettsia

This Q fever presentation from Professor Stephen Graves is worthwhile of review.  The presence of Q fever in PNG is likely but not proven as yet.   Dr Ak’s paper to be appended soon!

Also review this summary of laboratory diagnosis of rickettsial infection from Prof Graves.

 

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Module 6: Central nervous system infections- case studies and references

  1. Acute meningitides – CNS infection cases Ferguson 2017 acute

2. Chronic meningitis and encephalitis  –  Encephalitis and chronic meningitis Ferguson 2017

See also this posting concerning cryptococcal antigen detection for HIV patients.

Potential viva questions (practice with each other!):

  • What are the causes of acute meningitis in adults … in children  … in neonates
  • What are the typical CSF findings in viral m … bacterial m.
  • What is a parameningeal focus and explain what CSF findings might be expected
  • Interpret this CSF picture – e.g one of the cases above
  • Discuss the laboratory diagnosis of cryptococcal meningitis
  • Discuss the lab dx of TB meningitis
  • What are viral envelopes made of ? Contrast the properties of enveloped and non-enveloped viruses.
  • Describe the causes of chronic meningitis
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UPNG May revision M Med sessions – presentations and further references

2nd May 2017

  1. UPNG Infection prevention and control including TB IC Ferguson– presentation

2.  UPNG 2 AMR including Bacterial genetics Ferguson  –  presentation

These two posting from our sister blog may help with understanding antibiotic classes:

3rd and 4th May

3. UPNG 3 Antibiotic usage and practical AMS Ferguson –  presentation

Example management approach to Staphylococcus aureus BSI – n.b. 60 events at PMGH in 2016 (40% MRSA)

Potential M Med projects list relating to the national AMR plan (discuss with your supervisors) : Potential projects!

Local antimicrobial resistance studies:

Osteomyelitis

  • Management of bone and joint infections due to Staphylococcus aureus. Davis-JS. Intern Med J. 2005 Dec;35 Suppl 2:S79-96.  An authoritative review.  Contact me if a copy required. 
  • Antibiotics for treating chronic bone infection in adults – Cochrane systematic review 2013:  poor quantity and quality of evidence; no evidence for IV superiority over oral. Old studies.

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HTLV-1 in Papua New Guinea

Guest posting: Dr Ian Marr, Senior Microbiology Registrar, Pathology North, NSW. 

Human T cell lymphotropic virus 1 (HTLV-1), the first human retrovirus discovered, is found in some PNG populations and is an important topic for M. Med. post-grads and established clinicians!

What is a retrovirus? What is the process whereby HTLV-1 infects human cells? And can you name other significant retroviruses that infect humans?

A retrovirus is a virus that has a single stranded positive sense segment of RNA. The virus carries a reverse transcriptase enzyme that  makes complementary DNA from the viral RNA once inside the host cell. This DNA is then incorporated into the host T lymphocyte genome for life.

Human T cell Lymphotrophic virus (HTLV) is in the genus Deltaretrovirus. There are currently 4 different types of HTLV. These are named sequentially, HTLV-1, HTLV-2, HTLV-3, and HTLV-4. Only HTLV1 and 2 have been seen in any large number in people, with HTLV-3 and 4 being found rarely. There is 65% correspondence between the DNA structure of HTLV-1 and HTLV-2.  Other significant retroviruses include HIV1 and HIV2!

HTLV-1/2 is 100nm in diameter and has a thin protein envelope. As detailed proviral DNA is integrated into host T lymphocyte DNA. Once these lymphocytes increase in number (e.g. in association with an inflammatory response) the HTLV viral load increases. HTLV-1/2 is unique in that it is difficult to find free viral RNA/DNA outside of the cell (unlike HIV), hence transmission of infection is thought to occur by transfer of the cells that carry virus internally. This may occur with blood product transfusion. 95% of the provirus (dsDNA) is located in CD4+ T lymphocytes, and the rest in CD8+ T cells and dendritic cells. See this article for a good explanation whereby HTLV-1/2 infects T cells.

In 1999 HTLV-1 was found in PNG in the Madang, Chimbu and Enga regions.

What were the prevalence rates in Madang from this study? Where else in the world is HTLV1 and 2 found? 

Madang had the highest prevalence from this study conducted in 1999. It showed 39 out of 267 tested were positive for HTLV-1 antibodies on Western Blott analysis.

HTLV1 and 2 are found in clusters around the world. HTLV-1 is found in PNG, Melanesia, Solomons, central Australia, central Africa, the Caribbean, Brazil, and southern Japan. PNG, Melanesia and central Australia have a unique subtype named ‘c’ [HTLV-1c]. The significance of this subtype on clinical outcomes is not clear.

HTLV-2 is found in the Americas. Certain subtypes of the virus predominate in different countries.

What diseases have been associated with HTLV1/2?

The diseases associated with HTLV include:

  • Malignancy – Adult T cell leukemia/lymphoma (ATLL). This T cell associated malignancy occurs after 20-30 years of infection with HTLV-1 and has four different clinical presentations which display varying speed of onset: 1) acute, 2) lymphomatous, 3) chronic, and 4) smouldering. It is estimated that 2-4% of chronically infected HTLV-1 persons will develop ATLL. Survival is poor although treatment is still available in the form of chemotherapy.
  • HAM (HTLV-1 associated myelopathy – also known as Tropical spastic paraparesis – [TSP]). This is a degeneration of the spinal cord that causes a spastic transverse myelitis involving predominantly the lower limbs and impaired bladder function. It is estimated that 0.25-3.7% of chronically infected HTLV-1 persons will develop this syndrome. Symptoms do not present until at least 30-40 years of HTLV-1 infection. The current hypothesis behind the mechanism of damage is that the neuronal and glial cells are destroyed as a ‘bystander effect’, whereby the infected close by CD4+ T cells are targeted by cytotoxic T cells for destruction and the toxic cellular contents and effect of cytotoxic T cells damages the surrounding neurons. This is yet to be conclusively proven. There are some treatments (all with little evidence that are used to help). These include corticosteroids, and Interferon alpha and beta. See attached article on HAM.
  • Strongyloides – HTLV-1 has been associated with disseminated strongyloidiasis that reoccurs.
  • Dermatitis – HTLV-1 associated infective dermatitis (HAID) is the most common presentation in children. It is characterised by chronic eczema like eruption with persistent Gram positive skin infections.
  • Blood stream infection -. There are increased rates of blood stream infection in those infected with HTLV-1.
  • Bronchiectasis – HTLV-1 has been shown to be associated with bronchiectasis

What are the most common methods of HTLV-1 spread in communities?

3 major routes for infection:

  • mother-to-child transmission (mostly with breast-feeding)
  • sexual transmission
  • transfusion of cellular blood products infected with HTLV-1

What are the techniques for testing for HTLV1 and 2?

Methods of testing include screening for antibodies produced in defense of infection. This typically involves an enzyme immunoassay (EIA) which is then confirmed by a western blot (see references).

Pro-viral DNA can be detected in these cases but is often left only for research purposes.

References

  1. Takao et al. Journal of Clinical Virology, Seroprevalence of human T-lymphotropic virus type 1 in Papua New Guinea and Irian Jaya measured using different Western blot criteria.  
  2. Lab tests online HTLV 
  3. Buxton et al. NRL, Presentation: HIV-1 western blot interpretation/analysis
  4. McGill et al 2012.  HTLV-1-associated infective dermatitis: updates on the pathogenesis 

Image reference – http://plaza.ufl.edu/roxanna/HTLV%20projects.htm

HTLV1 prevalence 2005

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