5. New and threatening diseases
New infections -“Emerging”
new infectious diseases arise as a result of the
emergence of unidentified infectious agents
Threatening infections–“Re-emerging”
threatening infectious diseases, the result of the
repeated or more frequent appearance of
already known infectious agents
6. The term new infections implies
• Infection of a new host population with a
known infectious agent
• A completely new infectious agent and a new
disease
• A new infectious agent that causes an already
known disease
• A more complicated clinical picture of the
disease caused by a known infectious agent
7. The term threatening infections implies
• Increased incidence of disease
• Change in the geographic distribution of
diseases
• Increasing resistance and emergence of
multiresistant infectious agents
8. Factors that contribute to the emergence
of new and threatening diseases
1. Demographic and behavioral factors
Overpopulation
Risky sexual behavior (HIV, STDs)
Drug use (HIV, hepatitis C)
Dietary changes: international cuisines (foodborne
infections)
Greater number of immunocompromised: elderly,
HIV/AIDS, malignancies, use of antibiotics and other
drugs
9. 2. Technological development and industrialization
o Mass production of food
o Use of antibiotics in food production
o In Medicine: Extending Human Life (IC)
3. Economic development, changes in ecosystems and land
use
o More frequent exposure to wild animals and disease
vectors (Lyme disease....)
o Changes in ecosystems due to industrialization
Factors that contribute to the
emergence of new and threatening
diseases
10. Factors that contribute to the
emergence of new and threatening
diseases
4. International travel and trade
The possibility of easy transmission of exotic
pathogens - air traffic
Import of food, etc. - a possible way of transmitting
pathogens
5. Adaptations and changes of microorganisms
The development and spread of resistance - a
consequence of excessive use of antibiotics
Increase in virulence
Change of host – (from animals to humans)
11. Factors that contribute to the
emergence of new and threatening
diseases
6. Failures in prevention and health protection
measures
Absence of infection control
Inadequate reporting of illness
Infrastructure: water supply, sewerage...
Inadequate or absent vaccination
Control of vectors - insects, e.g.
12. Additional factors contributing to the
emergence of these diseases in the new
millennium
7. Climate changes
8. Poverty
8. Wars and starvation
9. Use of biological weapons
13. Imported diseases
Diseases that are not autochthonous in a certain
geographical area
and or
diseases caused by strains of microorganisms
that are not autochthonously present in a
certain area
14. Tourism - risk of disease
• It depends on the destination
• Tropical and subtropical regions
• - the most common source of infections
(underdevelopment, climatic conditions and endemic
foci)
• 22 - 64% of travelers from the tropics have health
problems caused by imported diseases upon return (US
data)
• Developed countries - sometimes a source of
multiresistant pathogens, diarrheal infections (ETEC,
EHEC...) and less often others
15. Risk factors for imported diseases
INGESTION
• Defective water
Hepatitis A and E, Salmonella, Shigella, Giardia,
Poliomyelitis, Amebiasis, Cryptosporidiosis, Cholera,
Typhoid
• Unpasteurized dairy products
brucellosis, Salmonella, Shigella, Listeria monocytogenes,
Q fever
• Thermally unprocessed food
Salmonella, Shigella, E.coli, Campylobacter, trichinosis,
helminthiasis, amebiasis, toxoplasmosis
16. THE ENVIRONMENT
• Water - leptospirosis, schistosomiasis,
Acanthamoeba, Naegleria spp.
• Soil - anthrax, helminthiasis, cutaneous larva
migrans
• Air - influenza, measles, tuberculosis
• Sexual contact - HIV, hepatitis B and C, syphilis,
gonorrhea, herpes
• i.v. drug addicts/transfusion – HIV, hepatitis B
and C, malaria, toxoplasmosis, babesiosis
• Contact with a sick person - TB, EBV, meningitis,
lasa, pneumonia
22. Enterococcus spp.:
– VRE – vancomycin resistant enetrococcus
– HLAR – high level of animoglycoside R
– Penicillin resistance
Streptococcus pneumoniae:
– PRP – penicillin-resistant pneumococcus
– NSPS – penicillin not sensitive pneumococcus
– MDRP – multi resistant (macrolides,
fluoroquinolones.....)
23. Enterobacteriaceae
– ESBL (extended spectrum beta lactamase)
plasmid beta lactamases that lead to
resistance to all beta lactams except
carbapenem (therapy of choice) – most often
present in E.coli, K.pneumoniae, Proteus
mirabilis
– Resistance to aminoglycosides
– Resistance to fluoroquinolones
24. Non-fermenting Gram-negative bacilli
MBL (metallo beta lactamase)
resistance to all beta lactams except
monobactam
Acinetobacter spp. – multiresistance
– Panresistance
other resistant pathogens....
– gonococcus, meningococcus, H.influenzae....
25. Threatening bacterial infections
• Tuberculosis
- number of cases
– resistance - MDR TB (multi drug-resistant TB)
– Synergy with HIV infection
27. • Diarrheal infections
E. coli (EHEC)
– The most important cause of bloody diarrhea and kidney
syndrome in developed countries - we have no data
Salmonella
– Europe: Salmonella serotype Enteritidis is dominant
Campylobacter spp.
– Frequent infections worldwide
Vibrio cholerae
– increase in incidence in endemic areas, possibility of
importation
Threatening bacterial infections
28. • Infections caused byStreptococcus pyogenes
– Increasing incidence and severity of clinical
forms of the disease
• Legionnaires' disease
• Meningococcal infections (vaccine)
• Lyme disease
• Diphtheria
Threatening bacterial infections
32. SARS
• SARS Corona virus (Coronaviridae)
• Mortality high in the elderly (over 60 years old)
• Transmission:
- direct contact with the patient
- the droplet way
-feco-oral route (!?!)
Diagnosis
- PCR, isolation in cell culture
33. Influenza (flu)
Influenza pandemics in the 20th century
recombinants of bird flu virus and human influenza virus
1918 – H1N1
1957 – H2N2
(Asian flu)
1968 – H3N2
(Hong Kong)
1977 – H1N1
(Russian flu)
37. 1. Togaviridae (Eastern equine encephalitis
virus, Western equine encephalitis virus,
Venezuelan equine encephalitis virus)
2. Flaviviridae (Yellow fever, Dengue, West
Nile encephalitis, Tick-borne encephalitis)
3. Bunyaviridae (Crimean-Congo hemorrhagic
fever, Rift Valley fever)
Arbovirus infections
38. Arbovirus infections
Clinical manifestations
Fever and rash - non-specific clinical picture (flu-like,
rubella), development of hemorrhagic fever or
encephalitis.
Encephalitis
Hemorrhagic fever
Diagnosis
- Serological - detection of IgM antibodies
- Virological - PCR, IF, isolation in living cell systems (BSL 3 and 4)
39. Arbovirus infections in Europe and
Serbia
Crimean-Congo hemorrhagic fever
Reservoir: mammals
Transmission: ticks (Ixodes)
*Kosovo 2001 – 69 sick, 5 died
2002 – 12 sick, 3 died
Tick-borne encephalitis
Reservoir: mammals, birds
Transmission: ticks (Ixodes)
* Data for YU (from the 60s)
40. Arbovirus infections in Europe
(Serbia !?!)
West Nile encefalitis
Reservoir : birds
Transmission: mosquitoes
*Data for Serbia (from the 70s)
41. Arbovirus infections in Europe (Serbia
!?!)
Dengue (Dengue hemorrhagic fever)
Reservoir: primates - monkeys
Transmission: mosquitoes
*Recent cases in Europe
(Greece, 1927-28)
42. Viral zoonoses
Definition:
Animal diseases that can be transmitted to
humans
Transmission:
1. Direct - rabies, lassa, ebola and marburg,
hantaviruses
2. Indirectly (via vectors) - arboviruses
44. Haantan virus infection
Hantaan virus (Bunyaviridae)
Hemorrhagic fever with renal syndrome (HFRS) -
mouse fever
* Vojvodina, Bosnia, South Serbia
Reservoir: rodents
Transmission: contact with fresh
or dried secretions and excretions
of infected rodents
Diagnosis
- Virological: PCR, IF, isolation in cell culture
- Serological: ELISA
45. Cyclospora spp.
Immature oocysts
10 µm
CDC
Epidemiology: contaminated fruit (raspberries) and
vegetables, water
Clinical picture: diarrhea
Diagnosis: finding of oocysts in the stool
Therapy: Bactrim® (trimethoprim-sulfamethoxazole)
46. Cryptosporidium parvum
Reservoir of infection: humans, mammals, reptiles,
birds, fish
Epidemiology: intake of oocysts from human or
animal feces - water, food, dirty hands
- they survive in feces for up to 6 months, sensitive
to +60°C, they are killed by freezing for 30 min
Clinical picture: diarrhea
Therapy: symptomatic
48. PLASMODIUM SPP.
• Plasmodium falciparum
• Plasmodium vivax
• Plasmodium malariae
• Plasmodium ovale
• MALARIA (paludismus – Latin: palus = swamp, swamp
fever)
• Vector – Anopheles spp.
• ABOUT 270 MILLION PEOPLE IN THE WORLD ARE
SICK OF MALARIA, AND ABOUT 2.5 MILLION DIE A
YEAR, 3.2 billion people live at risk
• P. falciparum and P. vivax - 95% of infections
49. Malaria – Life cycles
(Iz: White NJ. Antimalarial drug resistance. Journal of Clinical Investigation 2004, 113:1084-1092., by Ken Beauchamp.)
50. MALARIA – WAY OF
TRANSMISSION
Via vector
Blood transfusion
Contaminated needles
From mother to fetus
51. MALARIA
• OVER 80 SPECIES OF ANOPHELES ARE POSSIBLE
VECTORS OF PLASMODIUM
• THERE ARE 7 SPECIES PRESENT IN THE FORMER
YUGOSLAVIA
• A. maculipenis, A. superpictus, A. bifurcatus, A. algeriensis, A.
plumbeus, A. sacharovi i A. hyrcanus
• CLINICAL PICTURE
MALARIA ATTACK WITH PROGRESSIVE
ANEMIA AND THE APPEARANCE OF
SPLENOMEGALY
A MALARIA ATTACK IS A SET OF PAROXYSMS
BETWEEN WHICH SHORTER OR LONGER
AFEBRILE INTERVALS OCCURS
52. MALARIA
• paroxysms are the result of the simultaneous
spraying of a large number of erythrocytes and the
release of merozoites into the blood
• the paroxysm clinically begins with a fever (several
hours), followed by a febrile stage (t° of the
continuous type and over 40°c, several hours) and
ends with a sudden drop in t° (crisis) with profuse
sweating
54. MALARIA /DIAGNOSIS
CLINICAL PICTURE
SPECIFIC DIAGNOSIS
• PROOF OF THE PRESENCE OF PARASITES
• SEROLOGY
• PCR
MATERIAL USED IN DIAGNOSTICS :
• BLOOD (INCLUDING CORD BLOOD)
• BONE MARROW PUNCTATION OR, EXCEPTIONALLY, THE
LIVER
• PATHOHISTOLOGICAL TISSUE PREPARATIONS OF
VARIOUS ORGANS
BLOOD: BLOOD SPREAD AND THICK DROP
THE RULE IS TO TAKE BLOOD AS OFTEN AND AS EARLY
AS POSSIBLE, USUALLY FOR 3 CONSECUTIVE DAYS IN
THE MORNING AND EVENING, THAT IS MORE TIMES
DURING THE DAY AND NIGHT!!!
55. Rapid diagnostic tests for malaria
Detection of malaria parasite Ag
(immunochromatographic tests)
HRP-2 (protein rich with histidin) – for P. falciparum
pLDH (lactate dehydrogenase)
56. MALARIA - QUESTIONS
1. 3 words when it`s time to think about MALARIA?
Travel
Fever
Emergency
2. 3 decreasing biological parameters during uncomplicated
MALARIA?
Glucosa
RBCs
Thrombocytes
57. MALARIA - QUESTIONS
4. 3 questions to tropical traveller before decision for prevention?
Where?
When?
How? (including questions about pregnancy, children)
5. 3 precautions to take to avoid malaria disease?
Avoid mosquito bites
Avoid Plasmodium infection - chemoprophylaxis
Avoid RBCs infection - post exposure prophylaxis
58. MALARIA – PROBLEMS !
• Parasite resistance to antimalarial
medications
• Mosquito resistance to insecticides
• There is no vaccine
• Imported malaria
59.
60. Questions and answers
1. Why did Ms. M.’s fevers occur in paroxysms (episodes)
of shaking chills followed by fever and then drenching
sweats?
During the course of malaria, the life cycles of the parasite
in red blood cells becomes synchronized so that large crops
of cells rupture to release merozoites at the same time.
When that occurs, the parasite molecules responsible for
inducing the inflammatory response become suddenly
abundant in the blood. That causes the acute chills and
fever, which resolve when the free merozoites are cleared
from the bloodstream or enter other red blood cells. The
sweat occurs when the hypothalamic thermal set point is
lowered and the body must lose heat to bring the
temperature down.
61. Questions and answers
2. Why did she have dark urine?
Malaria induces red blood cell hemolysis. That occurs
because of direct infection and destruction of cells to be
sure, but more importantly, the infection also induces an
autoimmune hemolysis that is responsible for most of the
red blood cell loss.
3. Why did she develop edema of the lungs and an
elevation of the serum creatinine?
Plasmodium falciparum is the species of malaria most likely to
induce dysfunction of organs like the lung (edema), kidney
(increased creatinine and decreased glomerular filtration
rate), and brain (cerebral malaria) because the mature
parasites make the parasitized red blood cells adhere to
vascular endothelial. That stickiness impedes blood fl in
capillary and small venular beds, causing ischemia and
hemorrhage.
62.
63. Questions and answers
1. How and when did Ms. A. most likely become infected
with Mycobacterium tuberculosis?
Exposure most likely occurred years earlier when Ms. A.
was on the AIDS ward in South Africa. At that time, she
was exposed to patients with active, untreated tuberculosis
who were coughing and thus creating aerosols of M.
tuberculosis in droplet nuclei. Ms. A. inhaled the droplet
nuclei and developed a primary infection in the lung that
resolved after she developed an immune response.
2. Why did it take so long for Ms. A. to develop active
tuberculosis?
Until recently, her cellular immune response controlled the
organism. When hypersensitivity against the organism
created a cavity in her lung, her immune system lost
control.
64. Questions and answers
3. By what route did the tubercle bacilli most likely arrive
at the apices of her lungs?
Organisms in aerosolized droplet nuclei were ingested by
alveolar macrophages in the lower parts of the lung where
the primary infection occurred. Some bacilli were then
carried by the bloodstream and lymphatics (during the
lymphohematogenous dissemination phase) to the well-
aerated apices of the lungs where the bacilli grow more
abundantly.
4. Which individuals are most likely to develop active TB
from contact with Ms. A.?
Among the various persons with whom she has contact,
the risk is greatest for the infants (<1 year of age) at the day-
care center.
65. Questions and answers
5. How would her illness have differed if she had had
AIDS?
If she had had both AIDS and tuberculosis, the tuberculosis
would have progressed more rapidly. She would have been
more likely to have disseminated tuberculosis involving
multiple organs, and she would not have developed
cavities in the apices of her lungs. Pulmonary cavitation is
due to a vigorous hypersensitivity reaction to the
organisms that is impaired or absent in AIDS.
