Diseases possibly encountered through Migrational Influx
Filip Moerman.Infectiologist
December 8th, 2015
Overview of this presentation
• Multi‐drug‐Resistant Tuberculosis• “MERS”• High level Antibiotic Resistance: “CPE”• Non‐falciparum malaria• Chagas’
disease
• Infection with Strongyloides stercoralis
Definitions
What is resistant tuberculosis?
Treatment (no standard yet!!!)
In summary
Where do they come from?
Belta‐TBnet
High cure rate in Belgium•67.2% (2001‐2004) to 84.4% (2005‐2010)•independent of •citizenship,•treatment history •and/or drug resistance pattern.•Multi‐disciplinaryapproach•Easy access is provided to second‐line drugs•Full MDR‐TB treatment is available at no cost to the patient•A network of field workers ensures home‐based management•Coordination of the information flow•OneregistrationsystemWHO Regional Office for Europehttp://www.belta.be/index.php?lang=french
Possible schemes. Duration: from 6, via 9‐12 to 20 months!
The Narcistic Doctor
New treatments
Sirturo®. Long half‐life!! Won a price recently: “best new drug”
Delamanid (Deltyba©)
Back in the picture: SURGERY
Advantages• Rapid bacterial conversion• Removal of mycobact load• Increased chance of cure:
up to 90% if followed by adequate therapy in MDR‐
TB; more than 50% cure rate with XDR‐TB.
Pomerantz, et al.J Thor cardiovasc surg 2007.
Risks • Increased if BMI < 18.5• Morbidity and mortality
exist: fistulas, resp failure, empyema, wound infection
• Long term functional deficit• Transfer in HC settings• Cost
Facts and figures
• There is no treatment for MERS• First case in 2012• September 2015: 1591 cases, 571 died• South‐Korean outbreak 4 May 2015: country with
the largest number: 186 cases in July 2015 of which 36 died (CFR 19%) (Lim, et al. Trans R Soc Trop Med Hyg 2015)
• Interhuman transmissibility exists, but no pandemic potential yet (Breban et al. Lancet 2013)
Transmission paths
Emeergency dpt: be prepared!
Case definitions (!) (Belgian gvt)
Malaria
Disease caused by :
• Plasmodium
falciparum• Plasmodium vivax• Plasmodium ovale• Plasmodium malariae
• Rarely infection with zoonotic parasites
Malaria
cycle
Liver schizont
Hypnozoit
Within 30’
: Penetration of liver
cells.
Asexual multiplication
in liver cell
1. Nuclear division
2. Cytoplasm division
Life cycle
• P. vivax
and P. ovale
: some liver parasites become dormant
• Hypnozoites : responsible for late relapse
Malaria : geographical distribution
• P. falciparum
: mainly tropical – most frequent species in sub Saharan Afrika (95%)– South East Asia – Latin America (Central Am 1%, South Am ± 40%)– Oceania
• P. vivax
: biggest area (to polar circle)
• P. ovale
: mainly West‐Africa (only in Duffy blood group neg)
• P. malariae
: widely spread but rare infections
• Zoonotic malaria is rare
Malaria : Physiopathology
• Hemolysis– Fever– Flue‐like myalgia (GBP)– Pale – Anemia – Dark urine– Splenomegaly– Reticulocytosis– Thrombocytopenia
Treatment of P. vivax/ovale
Chloroquine, except Indonesia and Papoea New Guinea: Atovaquone + Proguanil HCl, followed
by Primaquine (twice 15 mg q14/7), to eradicate the Hypnozoites.
Vienna dec 2013: Prof David Livermore• Dramatic call to stop prescribing antibiotics
empirically
(exc the septic pt)• Are we heading back to the pre‐war era?• Big threat from India (1/3 of the world’s pop)• General rule: decolonisation/eradication only
works in 50% and its usefulness hasn’t been proven.
• Example: Gonorrhea (1930 Sulpha, 50‐60 Peni, 70 Peni+, FQ 90, now C3 (ev + Azithro),
later Solithromycine?
Resistance
• Definition• Detection: phenotypic (MIC), disc diff (+ breakpoints)• Currently via genetic testing (eg PCR)• Mechanisms: mutations of genetic bact material.
Vertical transmission may occur• Or: via plasmids (vert + horiz transm): quicker
dissemination. • Causes of resistance: multiple & complex
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Bloodstream infections due to Oxa‐48‐ like Carbapenemase Prod Enterob,
• Very important paper (Balkan et al. Int J of Infect Dis 2014). CPE is the big threat!!
• The optimal treatment remains undefined• But for sure: Colistin‐based dual combinations• Importance of rectal screening (early
recognition and prompt treatment)• Isolation if screening positive!! (All pts coming
from…..???)• High [excess] mortality rates (!)
Carbapenemases (non exhaustive)
What about the future?
• Not looking well; Livermore speaks of an impending catastrophe!
• AB‐pressure MUST decrease, Quit Empiric!!• Screen as pre‐test‐probability (origin, geography,
underlying illnesses ;..) on multi‐R is high• Concerted action required.• Awareness of the population: no AB ≠
slower
healing (viral, bacterial); lower immunity then lower threshold for AB (as for sepsis)
• “10‐by‐20‐initiative”, but will it be true = ?
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Chagas’ disease
– Only in South‐America
– Transmission via faeces of ‘blattes’
(Kakkerlak, Beetle)
– Congenital transmission
– Transmission via blood transfusion
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Chagas’ diseaseTrypanosoma cruzi
Oswaldo Cruz & Carlos Chagas
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Vectors
• big (2‐3 cm)
• lives 2‐5 j
• night biters (±10‐25’)
• painless
• Defaecation during bite
• liquid faeces
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Symptoms: chronic
• Oesophagus
:– Dysphagia because of mega‐oesophagus
• Heart lesions
: – apical aneurysm, arythmia, conduction disorders– Heart failure– No coronaropathy– Embolic disease : CVA, leg, bowel infarctus, kidney infarctus,
…
• Colon :
– Constipation because of mega‐colon
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Charles Darwin
megacolon
Nematodes:
Strongyloides stercoralis• In humans : parthenogenesis• In nature : sexual replication• Auto‐infection: transcut. or transmucosal
• Larva currens : pathognomonic• Chronic “Loeffler”• Protein‐loosing enteropathy (S. fuelleborni)• HTLV‐1 en Steroiden : hyperinfection : skin, brainIntestines, lungs, ….
• Diagnosis
: copro, Baerman, sputum, serology(positive ONLY after 1 year!), eosinophilia not always• R/ iveremctine, albendazole (niet mebendazole)
Ei van Strongyloides stercoralis
Extremely dangerous in immunosuppression: AIDS, Chemo, Krohn/Colitis, Steroids, …
Areas with high incidence rates of Strongyloides stercoralis
infection
MicroscopyRhabditoid first‐stage (L1) larvaeThe first‐stage rhabditoid larvae (L1) of Strongyloides stercoralis
are 180‐380 µm long, with a short buccal canal, a
rhabditoid esophagus and a prominent genital primordium.
These L1 larvae are usually found in stool, as the eggs
embryonate and hatch in the mucosa of the small intestine of the
host.
They may also be found in soil and cultured feces
Infective, third‐stage filariform larvae (L3) of Strongyloides stercoralis
are up to 600 µm long. The tail is notched and the esophagus to intestine
ratio is 1:1. Infective L3 larvae are found in soil and invade the human host by direct penetration of the skin. They may be found in respiratory
specimens during cases of autoinfection.