Emerging infectious diseases

Click here to load reader

download Emerging infectious diseases

of 46

description

-SIr ZYbs

Transcript of Emerging infectious diseases

  • 1.EMERGING INFECTIOUS DISEASESAnthrax (Bacillus anthracis),Staphylococcus aureus , and Influenza (A(H5N1))

2. ANTHRAX (Bacillus anthracis) -2001 ANTHRAX (Bacillus anthracis) Bacillus anthracis was isolated by Robert Koch in1877. It is endospore forming. Endopsore is a resting structure formed insidesome bacteria. It is aerobic and gram positive. It is able to grow in soil types with specificmoisture conditions. 3. B. anthracis in Human Lung Capillary 4. ANTHRAX (Bacillus anthracis) -2001 ANTHRAX (Bacillus anthracis) The endospore can survive for up to 60 years insoil. It is found in grass and could be eaten by sheepand cattle causing fatal sepsis. Anthrax infection with these scenario is rare in theUS. But recorded cases of infection from animalproducts (wool and hides) from the Middle Eastby buyers in importing countries are known. 5. ANTHRAX (Bacillus anthracis) -2001 ANTHRAX (Bacillus anthracis) PROCESS OF INFECTION Endospores are phagocytized by macrophage. Endospores change into their active state. Bacillus anthracis multiplied eventually killing thecell. It gets out of the cell and finds its way to thebloodstream. Then it secretes certain toxins. 6. ANTHRAX (Bacillus anthracis) -2001 ANTHRAX (Bacillus anthracis) The virulence is the result of 2 endotoxins. The 2 endotoxins share a 3rd toxic component. The 3rd toxic component is called a Protectiveantigen. This protein protective antigen component bindsto cell-receptors. The endotoxins attached to the protectiveantigen. Protective antigen binds to target cells andpermits entry. 7. ANTHRAX (Bacillus anthracis) 2001 ANTHRAX (Bacillus anthracis) THE 2 ENDOTOXINS 1. EDEMA TOXIN Causes local edema (swelling). Interferes with macrophage phagocytosis. 2. LETHAL TOXIN Targets and kills macrophages. Disables defense of the host cell. 8. MACROPHAGE ENGULFINGBACTERIUM 9. ANTHRAX (Bacillus anthracis) -2001 ANTHRAX (Bacillus anthracis) THE CAPSULE The capsule is made up of amino acid residuesand not of polysaccharides. It does not stimulate immune system response. It allows B. anthracis to mix with bloodundetected until their numbers reach millions perlitter. It then results to septic shock. 10. ANTHRAX (Bacillus anthracis) -2001 ANTHRAX (Bacillus anthracis) THREE FORMS IN HUMANS 1. CUTANEOUS ANTHRAX Happens when skin comes in contact withcontaminated material. Represents 90% of anthrax cases. The endospore enters minor skin lesions. Later a papule appears then vesicles and rupturesturning into an ulcerated area covered with blackeschar. In most cases pathogen does not enter bloodstream. Mortality is 20 % w/o antibiotic treatment and 1 % w/antibiotic. 11. ANTHRAX (Bacillus anthracis) -2001 ANTHRAX (Bacillus anthracis) THREE FORMS IN HUMANS 2. GASTROINTESTINAL ANTHRAX Caused by ingestion of undercooked food. Symptoms include nausea, abdominal pain andbloody diarrhea. Also ulcerative lesions mainly in the intestines butcan include mouth to throat region. The mortality could reach 50%. 12. ANTHRAX (Bacillus anthracis) -2001 ANTHRAX (Bacillus anthracis) THREE FORMS IN HUMANS 3. INHALATIONAL ANTHRAX (PULMONARYANTHRAX) Most dangerous form of anthrax. Endospores are inhaled in the lungs. High probability of entering the bloodstream isobserved in this form. For the first few days symptoms include mildfever, coughing, and some chest pain. Antibiotics can arrest infection at this stage. 13. ANTHRAX (Bacillus anthracis) -2001 ANTHRAX (Bacillus anthracis) THREE FORMS IN HUMANS 3. INHALATIONAL ANTHRAX (PULMONARYANTHRAX) Within 2 3 days infection, proceeds tobloodstream and results to septic shock. It kills the patient w/in 24 to 36 hours. Mortality reaches 100%. 14. ANTHRAX (Bacillus anthracis) -2001 ANTHRAX (Bacillus anthracis) ANTHRAX TREATMENT The treatment for anthrax includes ciprofloxacinor doxycycline. Prescription could last up to 60 days. 15. ANTHRAX (Bacillus anthracis) -2001 ANTHRAX PREVENTION Anthrax could be prevented by having vaccinationin endemic areas. The use of live attenuated vaccines in singledoses to livestock helps. The use of the inactivated form of anthrax withoutthe capability of forming protective toxins asvaccines are used safely for humans. Administered as 6 injections within 18 monthperiod followed by annual boosters. 16. ANTHRAX (Bacillus anthracis) -2001 ANTHRAX (Bacillus anthracis) Anthrax was used for bioterrorism. The current techniques for isolating andcultivating Bacillus anthracis is too slow. The US FDA developed a blood test that wouldjust take an hour. As protection against bioterrorism mails areinspected by automated electronic scanners forcontamination. 17. Staphylococcus aureus 1997 and1996 Staphylococcus It typically occurs as grapelike structures. Staphylococcus aureus is considered the mostimportant species. It is named for its yellow pigmented colonies. Aureus means golden. The species is a facultative anaerobe. It is considered to be pathogenic. 18. Staphylococcus aureus 19. Staphylococcus aureus 1997 and1996 Staphylococcus It grows well on high osmotic pressureenvironments and low moisture environments. It is found in nasal secretions in noses and skin. Also in high osmotic pressure foods like curedham and meats. And in low moisture foods. 20. Staphylococcus aureus 1997 and1996 Staphylococcus Staphylococcus produces toxins. Surgical wound infection of Staphylocccus aureusin hospitals become a common problem. It quickly develops resistance to penicillin. It is also responsible for producing the toxin thatcauses toxic shock syndrome. Toxic shock syndrome is characterized by feverand vomiting and could lead to death. 21. Staphylococcus aureus 1997 and1996 Staphylococcus It is has enterotoxin that causes vomiting andnausea when ingested. It causes food poisoning. 22. Staphyloccus aureus 1997 and1996 2 TYPES OF Staphylocccus aureus 1. Staphyloccus aureus (VRSA) VR in VRSA stands for Vancomycin resistant. Emerged in 1996. This type poses a serious threat to patient care. 2. Staphylococcus aureus (MRSA) MR in MRSA stands for Methicillin Resistant. Emerged in 1997. 23. Staphyloccus aureus 1997 and1998 VANCOMYCIN ANTIBIOTIC What is Vancomycin? Vancomycin is one small group of glycopeptideantibiotics derived from a series of Streptomycesfrom Borneo. Vancomycin toxicity was a serious problem. But improved purification procedures correctedthis. 24. Staphylococcus aureus 1997 and1996 VANCOMYCIN ANTIBIOTIC The vancomycin has a very narrow spectrum ofactivity. It works by inhibiting cell wall synthesis of thebacterium. The antibiotic is extremely important inaddressing the problem of MRSA. It is considered to be the last line of defense forStaphyloccus aureus infection. 25. Staphylococcus aureus 1997 and1996 VANCOMYCIN ANTIBIOTIC Use of Vancomycin led to the selectionvancomycin resistant enterococci. (VRE) The Vancomycin resistant enterococci areopportunistic gram negative bacteria. They are troublesome in hospital settings. Vancomycin resistant pathogens leaves almostno alternative and is therefore considered amedical emergency. 26. Staphyloccocus aureus 1997 and1996 METHICILLIN ANTIBIOTIC The first semisynthetic penicillin designed toevade action of penicillinases. The strains of staphylococci developed resistanceto methicillin. The resistance became so prevalent thatmethicillin has been discontinued for use in theUS. It is replaced with oxacillin and natcillin. 27. INFLUENZA (FLU) INFLUENZA VIRUS In developed countries they are very much awareof the flu. Flu is characterized bychills, fever, headache, and general muscularaches. Recovery takes a few days. The cold like symptoms appear as feversubsides. 50, 000 to 70, 000 Americans die every yearbecause of this viral infection. Diarrhea and intestinal discomfort are not a 28. INFLUENZA VIRUS 29. INFLUENZA (FLU) INFLUENZA VIRUS It has 8 segments of RNA. The RNA is enclosed with protein. The virus has outer bilipid layer. Projections are found outside the virus. The projections are: 1. The H hemagglutinin spikes - numbering upto 500 and responsible for recognizing andattaching to body cells. 2. The N-neuraminidase spikes numbering upto 100. 30. INFLUENZA (FLU) INFLUENZA VIRUS The antibodies are directed at these spikes. Hemagglutination reaction test utilizes this spikes. N spikes differ in appearance and function to Hspikes. The N spikes enzymatically help the virusseparate from the infected cell. N spike also stimulates antibody formation. 31. INFLUENZA (FLU) INFLUENZA VIRUS The viral strains of influenza are identified by theirvariation in H and N antigens. There are 15 subtypes of H antigens and 9 subtypesof N antigens. A strain is a result of substantial alteration in theprotein make-up. Alteration happens due to Antigenic Shifts. Influenza that underwent antigenic shift evades mostof immunity developed in humans. Antigenic shifts resulted to the 1918, 1957 and 1968pandemics. 32. INFLUENZA (FLU) INFLUENZA VIRUS The influenza virus was not isolated before 1933. Therefore antibody analysis was used todetermine viral genetic make-up. Antigenic shifts are due to geneticrecombinations. There is recombination or reassortment of RNAbetween animal (swine, horse, birds) and humanstrains. Swine most especially could be infected by bothhuman and fowl. Chinese farming communities are considered tobe mixing vessels of the viral strains. 33. INFLUENZA (FLU) INFLUENZA VIRUS Wild ducks and migratory birds becomesymptomless carriers. Southeast Asian Poultry houses becomebreeding grounds for the H5N1 strain that killed 6in Hongkong in 1997. Strains became efficient in human to humantransmission. 34. BIRD FLU VACCINATION 35. INFLUENZA (FLU) EPIDEMIOLOGY OF THE INFLUENZA Antigenic drift Minor annual variations. Happens b/n major antigenic shifts. E.g. H3N2 strain could have minor changes. Like a single amino acid alteration. (Change in Nor H) This type of new H3N2 will be named from thelocality were it is discovered. 36. INFLUENZA (FLU) EPIDEMIOLOGY OF THE INFLUENZA Antigenic drifts are responses to selectivepressure by antibodies. (IgA) It is estimated that there is 1 mutation in eachmillion multiplication of a virus. Viral RNA is characterized by high mutationrates, reason include it not having a proof readingability. Vaccines circulating for 10 years become lesseffective due antigenic drifts. 37. INFLUENZA (FLU) EPIDEMIOLOGY OF INFLUENZA Virus is also classified according to protein coats. A responsible for major pandemic. B geographically limited and infections are rare. C milder infections. The mortality of influenza is 1%. The very young and old are susceptible. But in major epidemics, deaths are often large. 38. INFLUENZA (FLU) INFLUENZA VACCINE Long-term immunity vaccine is impossible. The viral strain is identified early usually inFebruary so that vaccine for this strain will beavailable next year. Viral strains are collected in 100 centersworldwide. Viral analysis is used to decide vaccinecomposition for the next flu season. Vaccine is usually multivalent and are directed at3 most important strains. These are grown in embryonated egg cultures. 39. INFLUENZA (FLU) INFLUENZA VACCINE The vaccine is 70 to 90% effective and theprotection is good for 3 years. A Nasal spray vaccine is available for ages 1 to 5years. Vaccine development is difficult. The egg-embryo culture is clumsy and laborintensive. It requires extended time. There is poor growth of the virus. And the viral strain could kill the embryo. 40. INFLUENZA (FLU) INFLUENZA VACCINE A solution to vaccine development will be the useof reverse genetics technology. Viral RNA is converted to DNA and DNA is turnedto RNA. In the DNA change there is pathogenic generemoval. A benefit of this technique is the minimization ofharmful contamination. 41. INFLUENZA (FLU) INFLUENZA VACCINE In 1918 and 1919 up to 20 million died. The young adults had the highest mortality. Death ensues within a few hours. Aside from respiratory tract infection it also movesto lungs causing viral pneumonia. Evidence also suggests that other organs of thebody are affected. 42. 1918 FLU PANDEMIC 43. INFLUENZA (FLU) INFLUENZA VACCINE A 2005 analysis of a US soldier and Alaskanvictims lead to the complete genetic sequencingof the 1918-1919 flu virus. The virus was recreated and grown in mice andchicken embryos. The Avian virus had 10 amino acid changes. The developed lethal gene allowed the virus toattached to lungs. Bacterial complications also accompanied the flu. The strain became endemic in swine in the US. 44. INFLUENZA (FLU) DIAGNOSIS OF INFLUENZA Diagnosis is difficult if based on clinicalsymptoms. Swab sampling of a physician could identify thevirus if its an A or B influenza within 20 minutes. This procedure is 70% sensitive and 90%specific. For viral strain identification, it is conducted inCentral laboratories. 45. INFLUENZA (FLU) TREATMENT OF INFLUENZA Amantadine and Rimantadine are antiviral drugsfor influenza. They significantly reduce symptoms of InfluenzaA. 2 drugs recently introduced are Zanamivir(Relenza) and Oseltamivir (Tamiflu) which areadministered orally. If taken 30 hours before the onset of symptoms itgreatly reduces symptom duration. Drugs should not be a substitute for vaccination. These drugs are amenable with antibiotic 46. END OF PRESENTATIONSir Zybrinskie T. Bangcado