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Infectious Disease 2 > (Re)Emerging Diseases > Flashcards

(Re)Emerging Diseases Flashcards

1
Q

Trends in infectious disease

A
  • Receded in Western countries 20th century d/t urban sanitation, improved housing, personal hygiene, antisepsis & vaccination
  • Antibiotics further suppressed morbidity & mortality
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2
Q

Trends since last quarter of 20th century

A

Unusually large number- Rotavirus, Cryptosporidiosis, HIV/AIDS, Hantaviraus, Lyme disease, Legionellosis, Hepatitis C

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3
Q

Define re-emerging infectious disease

A

Infectious agents that have been known for some time, had fallen to such low levels that they were no longer considered public health problems & are now showing upward trends in incidence or prevalence worldwide

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4
Q

Define emerging infectious disease

A

Newly identified & previously unknown infectious agents that cause public health problems either locally or internationally

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5
Q

Factors contributing to emergence

-Agent

A
  • Evolution of pathogenic infectious agents (microbial adaptation & change)
  • Development of resistance to drugs
  • Resistance of vectors to pesticides
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6
Q

Factors contributing to emergence

-Host

A
  • Human demographic change (inhabiting new areas)
  • Human behavior (sexual & drug use)
  • Human susceptibility to infection (Immunosuppression)
  • Poverty & social inequality
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7
Q

Factors contributing to emergence

-Environment

A
  • Climate & changing ecosystems
  • Economic development & Land use (urbanization, deforestation)
  • Technology & industry (food processing & handling)
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8
Q

Other factors contributing to emergence

A
  • International travel & commerce
  • Breakdown of public health measure (war, unrest, overcrowding)
  • Deterioration in surveillance systems (lack of political will)
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9
Q

List the factors influencing transmission of infectious agents from animals to humans

A
  • > 2/3rd emerging infections originate from animals- wild & domestic
  • Emerging Influenza infections in Humans associated with Geese, Chickens & Pigs
  • Animal displacement in search of food after deforestation/climate change
  • Humans themselves penetrate/ modify unpopulated regions- come closer to animal reservoirs/ vectors (Yellow fever, Malaria)
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10
Q

What climate and environmental changes influence emergence?

A
  • Deforestation forces animals into closer human contact- increased possibility for agents to breach species barrier between animals & humans
  • El Nino- Triggers natural disasters & related outbreaks of infectious diseases (Malaria, Cholera)
  • Global warming- spread of Malaria, Dengue
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11
Q

How does poverty, neglect, and health infrastructure affect emergence?

A
  • Poor populations are major reservoir & source of continued transmission
  • Poverty- Malnutrition- Severe infectious disease cycle
  • Lack of funding, Poor prioritization of health funds, Misplaced in curative rather than preventive infrastructure
  • Failure to develop adequate health delivery systems
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12
Q

What role does uncontrolled urbanization and population displacement play in emergence?

A
  • Growth of densely populated cities- substandard housing, unsafe water, poor sanitation, overcrowding, indoor air pollution (>10% preventable ill health)
  • Problem of refugees & displaced persons
  • Diarrheal & Intestinal parasitic disease, Lyme disease- Changes in ecology, increasing deer populations, suburban migration of population
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13
Q

What human behaviors affect emergence?

A
  • Unsafe sexual practices (HIV, Gonorrhea, Syphilis)
  • Changes in agricultural & food production patterns- food-borne infectious agents (E. coli)
  • Increased international travel (Influenza)
  • Outdoor activity
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14
Q

What are the causes of antimicrobial drug resistance?

A
  • Wrong prescribing practices
  • Non-adherence by patients
  • Counterfeit drugs
  • Loss of effectiveness seen in: community-acquired (TB, pneumococcal) & hospital-acquired (enterococcal, staphylococcal) as well as in antiviral (HIV, antiprotozoal (malaria), antifungal
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15
Q

What are the consequences of antimicrobial drug resistance?

A
  • Prolonged hospital admissions
  • Higher death rates from infections
  • Requires more expensive, more toxic drugs
  • Higher health care costs
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16
Q

Causative organism of anthrax

A

Bacillus anthracis - gram positive, rod-shaped bacteria

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17
Q

Where is anthrax found?

A

Found naturally in soil and commonly affects domestic and wild animals around the world

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18
Q

How are animals/people infected with anthrax?

A
  • Rarely, people can get sick with anthrax if they come in contact with infected animals or contaminated animal products
  • Animals can become infected when they breathe in or ingest spores contaminated in soil, plants, or water
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19
Q

Anthrax infection in humans

A
  • Human get infected when anthrax spores get into the body
  • This can happen when people breathe in spores, eat food or drink contaminated with spores, or get spores in a cut or scrape in the skin
  • It is very uncommon for people in the US to get infected with anthrax
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20
Q

Where is anthrax more common?

A

In developing countries and countries that do not have veterinary public health programs that routinely vaccinate animals against anthrax

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21
Q

Explain the importance of anthrax in spore form.

A
  • When anthrax is disseminated as a biological weapon, it is disseminated as the spore form
  • When that spore enters either an open wound in the skin, the gastrointestinal tract, or the lung of a victim, it undergoes germination into the bacillus form as mentioned above
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22
Q

Where does germination and multiplication of anthrax occur in humans?

A
  • Especially in the inhalational form, this germination takes place in a macrophage
  • Anthrax is able to resist the destruction by macrophages
  • Once within this macrophage it is transported to a regional lymph nodes
  • Once the macrophage arrives at the lymph node the anthrax multiplies
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23
Q

What toxins are produced after anthrax multiplies?

A
  • Once it multiplies it produces two toxins, one called edema toxin and one called lethal toxin
  • These toxins cause massive amounts of tissue edema as well as tissue necrosis
  • *The growth of this bacteria, and the production of these toxins, produces the clinical picture of anthrax, and the eventual death of the patient with inhalational anthrax
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24
Q

Define anthrax toxemia

A

Toxemia is when the amount of anthrax toxin in the victim is enough to cause severe illness and/or death

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25
Q

List the 3 anthrax clinical syndromes

A
  1. Cutaneous
  2. Gastrointestinal
  3. Inhalational
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26
Q

Etiology of the 3 anthrax clinical syndromes

A
  • Typically the inhalation and GI forms carry a very high mortality rate
  • The cutaneous form of anthrax, which is the much more common and natural form of anthrax, typically has a very low mortality with antibiotic treatment
  • If left untreated, cutaneous anthrax can progress to creating a generalized infection that can also be fatal (approximately 20%)
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27
Q

How does GI anthrax develop?

A

After ingestion of contaminated, poorly cooked meat

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28
Q

Clinical presentation of GI anthrax

A
  • Abdominal pain, usually accompanied by bloody vomiting or diarrhea, followed by fever and signs of severe infection
  • GI anthrax is sometimes seen as mouth and throat ulcerations with tender neck glands and fever
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29
Q

Incubation and fatality of GI anthrax

A
  • Incubation period: 1–7 days

- Case-fatality: 25–90% (role of early antibiotic treatment is undefined)

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30
Q

Clinical presentation of cutaneous anthrax

A
  • Begins as a papule, progresses through a vesicular stage to a depressed black necrotic ulcer (eschar)
  • Edema, redness, and/or necrosis without ulceration may occur
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31
Q

How does cutaneous anthrax develop?

A

This form MC encountered in naturally occurring cases*

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32
Q

Incubation and fatality of cutaneous anthrax

A
  • Incubation period: 1–12 days

- Case-fatality: without antibiotic treatment: 20%; with antibiotic treatment: 1%

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33
Q

Clinical presentation of inhalational anthrax

A
  • A brief prodrome resembling a “viral-like” illness, characterized by muscle aches, fatigue, fever, with or without respiratory symptoms, nausea, vomiting, abdominal pain
  • As symptoms progress, more significant respiratory complaints develop, and patients may become significantly short of breath with complaints of air hunger.
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34
Q

Which symptoms suggest anthrax meningitis?

A

Confusion, neck stiffness, and headache suggest anthrax meningitis (seen in 50% of patients)

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35
Q

What is the incubation period for inhalational anthrax?

A

1-6 days

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36
Q

What symptoms occur during the terminal phase of inhalational anthrax?

A

Dyspnea, stridor, cyanosis, shock, chest wall edema, meningitis, widened mediastinum with effusion with overall toxic/septic clinical picture
*Death within 24 hrs if it reaches the terminal phase

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37
Q

Diagnosis of anthrax

A
  • Sudden onset of respiratory distress with mediastinal widening on x-ray
  • A small number of patients may present with GI or cutaneous anthrax
  • Gram stain of blood and blood cultures - but these may be late findings in the course of the illness
  • PCR and immunohistology testing may confirm diagnosis but samples must go to reference laboratory
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38
Q

Acute treatment of anthrax

A
  • Abx for most infections; inhalation anthrax is harder to treat and can be fatal.
  • Ciprofloxacin - 400 mg IV q 8 to 12 hr
  • Doxycycline - 100 mg IV q 12 hr
  • Antitoxin
  • Vaccination*
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39
Q

Post-exposure anthrax treatment

A
  • Oral prophylaxis
  • Ciprofloxacin (500 mg PO q12 h) X 60 days and until 3 doses of vaccine
  • Doxycycline (100 mg PO q12 h) X 60 days and until 3 doses of vaccine
  • Vaccination
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40
Q

Anthrax Vaccination

A
  • FDA approved 1970
  • Cell Free filtrate (NO organisms, dead or alive)
  • Adverse effects 1-3%
  • It is an immunization regimen that includes 6 injections.
  • For this vaccine to remain effective however the patient will require yearly boosters.
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41
Q

What organism causes the plague?

A

Yersinia pestis - a Gram negative, nonmotile, nonsporulating bacteria

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42
Q

Vector for the plague

A
  • Rodent flea: results in primary bubonic plague

- The plague bacteria can cycle between rats and their fleas.

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43
Q

When was the last plague outbreak?

A
  • The last urban outbreak of rat associated plague in US occurred in Los Angeles in 1924-1925.
  • Since that time plague has occurred in rural and semi rural areas of the western US where many types of rodent species are involved.
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44
Q

Clinical presentation of bubonic plague

A
  • Sudden onset of flu-like syndrome (fever, headache, rigors, malaise, myalgias, nausea)
  • Buboes formation - within 24 hours - swollen, infected lymph node (very painful!)
  • Cutaneous findings in 25% of cases
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45
Q

Incubation and mortality of bubonic plague

A
  • Incubation 1-8 days (mode 3-5 days)

- Mortality: Untreated60%; Treated < 5%

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46
Q

Pneumonic plague clinical presentation

A
  • 2 to 3 day incubation period
  • High fever, muscle aches, chills, headache
  • Cough with bloody sputum within 24 hours
  • Pneumonia progresses rapidly with shortness of breath, stridor, cyanosis, difficulty breathing, chest pain
  • Respiratory failure, shock, bleeding
  • Plague pneumonia and sepsis develop acutely and may be fulminant
  • Patchy lung infiltrates or consolidation seen on chest x-ray
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47
Q

Which form of plague is the most serious and can be spread person to person?

A

Pneumonic plague

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48
Q

Plague diagnosis

A
  • Gram stain and/or culture of lymph node aspirates, sputum, or CSF samples
  • Bipolar staining “Safety Pin” may be present
  • Immunoassays are also available
49
Q

Plague treatment

-antibiotic therapy

A
  • Streptomycin (choice) 15-30 mg/kg IM BID x 10 days
  • Gentamicin 2 mg/kg IV then 1.0-1.5 mg/kg q8h or 5 mg/kg IV q24h x 10 days
  • Doxycycline 200 mg IV then 100mg BID x 10-14 days
  • Ciprofloxacin - 400 mg IV q12h x 10 days
50
Q

Plague - control of secondary transmission

A

Standard, contact, and aerosol precautions for at least 48 hrs until sputum cultures are negative or pneumonic plague is excluded

51
Q

What is the world’s first eradicated disease?

A

Smallpox

52
Q

When were the last cases of smallpox?

A

1977- last endemic case in Somalia
1978- two laboratory cases in Britain
1980- WHO declares global eradication of smallpox

53
Q

Which pathogen causes smallpox?

A
  • Variola virus: an Orthopox virus, both minor and major forms of smallpox exist
  • Structure is a double stranded, large DNA virus
54
Q

Weaponization of smallpox vs. anthrax

A

It is not as easily weaponized as anthrax, and requires additional measures to afford the virus the stability in the environment

55
Q

Smallpox prodrome symptoms

A
  • Infection of respiratory mucosa
  • Minor viremia: seeding of liver, spleen
  • Major viremia: seeding of skin
  • Initial symptoms: acute onset fever, rigors, headache, vomiting- sometimes contagious
  • Virus cultured from blood
56
Q

Incubation of smallpox prodrome

A

Incubation 7-19 days (mean 12)

57
Q

Smallpox clinical presentation

A

-Early rash stage: enanthem = contagious
-Once sores in the mouth start breaking down: Exanthem
-Begins on face, hands, forearms
-Spreads to lower extremities
Centrifugal distribution*
-Macules –> papules –> vesicles –> pustules –> scabs/crusts –> scars
-Spreads to all parts of the body within 24 hours
-After about 4 weeks scabs have all fallen off, no longer contagious

58
Q

Management of smallpox contacts

A

-Immediate vaccination or boosting

VIG 0.6 ml/kg

  • Pregnant patients
  • Dermatoses patients
  • Creates passive immunity for that person*

STRICT quarantine x 17 days

59
Q

Smallpox vaccination

A
  • Employs Vaccinia virus
  • Given by scarification
  • One dose protective for 5-10 years
  • Must keep vaccinia immunoglobulin (VIG) on hand to treat complications of vaccination
60
Q

Complications of smallpox vaccination in normal host

A
  • Inadvertent Autoinoculation (skin, eye)
  • Generalized vaccinia
  • Erythema multiforme
  • Encephalitis
61
Q

Other complications of smallpox vaccination

A
  • Pregnancy: fetal vaccinia
  • Dermatoses/Burns: eczema vaccinatum
  • Immunocompromised: vaccinia necrosum
62
Q

Smallpox treatment

A
  • Public health emergency
  • Supportive care
  • Vaccinia Immunoglobulin
  • Strict quarantine until scabs off (at least 17 days)
  • Cidofovir
63
Q

What kinds of viruses cause Viral Hemorrhagic Fevers (VHFs)?

A

RNA viruses causing high fevers and generalized vascular damage

64
Q

Which viruses are VHFs?

A

Filoviruses (Ebola and Marburg)

65
Q

How are viral hemorrhagic fevers spread?

A

Human infections by insect bites or by contact with blood and body fluids

66
Q

Etiology of VHFs

A
  • RNA viruses causing high fevers and generalized vascular damage
  • May be spread by aerosol, on fomites, and by oral secretions and eye drainage in animals
  • Human infections by contact with blood and body fluids
67
Q

VHF pathogenesis

A
  • Fever, muscle aches, prostration
  • Cases evolve into shock and generalized mucous membrane hemorrhage
  • Conjunctival injection, petechial hemorrhage, and hypotension
  • Abnormal kidney and liver function tests: poor prognosis
  • Mortality varies; 50 - 80% Ebola Zaire
  • Disease severity and survival depends on various host factors; target organ is the blood vessel system
68
Q

S/sx of ebola virus

A
  • Fever
  • Severe headache
  • Muscle pain
  • Weakness
  • Fatigue
  • Diarrhea
  • Vomiting
  • Abdominal (stomach) pain
  • Unexplained hemorrhage (bleeding or bruising)
69
Q

Diagnosis of Ebola virus

A
  • To determine whether Ebola virus infection is a possible diagnosis, there must be a combination ofsymptoms suggestive of EVDANDa possible exposure to EVD within 21 days before the onset of symptoms.
  • Contact public health authorities is suspected disease.
  • Real time PCR testing for Ebola virus
70
Q

Treatment of Ebola virus

A
  • Supportive
  • Oxygen
  • Antipyretics
  • Antiemetics
  • Treat secondary infections if arise
  • No antiviral available
71
Q

Which pathogen causes marburg hemorrhagic fever?

A

Rousettus aegypti - fruit bats are considered to be natural hosts of the Marburg virus

72
Q

Etiology of marburg hemorrhagic fever

A
  • Causes severe viral hemorrhagic fever in humans
  • Fatality rates range from 24%- 88%
  • No specific antiviral treatment or vaccine is available
73
Q

How is marburg hemorrhagic fever spread?

A

Virus transmitted to people from fruit bats and spread among humans through human-to-human transmission

74
Q

Prevention of secondary viral hemorrhagic fever transmission

A
  • Animal studies indicate aerosol transmission possible
  • Single room with adjoining anteroom as only entrance
  • Handwashing station with decontamination solution
  • Negative air pressure room if possible
  • Strict barrier precautions (PPE)
75
Q

List the strict barrier precautions (PPE) for VHFs

A
  • Gloves, gown, mask. shoe covers, protective eyeware/faceshield
  • Consider HEPA respirator (e.g. N95) for severe hemorrhage, vomiting, diarrhea, cough
76
Q

Prevention of secondary viral hemorrhagic fever transmission cont…

A
  • Chemical toilet
  • All body fluids disinfected
  • Disposable equipment/sharps into rigid containers and autoclaved/incinerated
  • Double-bag refuse-outside bag disinfected
  • Electronic/mechanical equipment must be disinfected
77
Q

Diagnosis and tx of VHFs

A
  • Not usually made based on clinical findings; however, during outbreaks, clinical findings should trigger health care providers to isolate patients who may have symptoms
  • PCR and ELISA can detect later in the course of the disease
  • No specific treatment; supportive care, usually in ICU
78
Q

How is Dengue transmitted?

A

Dengue is transmitted primarily from human to human by the bite of theAedesmosquito

79
Q

Etiology of Dengue fever

A
  • Leading cause of illness and death in the tropics and subtropics
  • Nearly all dengue cases reported in the 48 continental states were acquired elsewhere by travelers or immigrants
  • Usually occurs during rainfall season when breeding is optimal for the Aedes mosquito
80
Q

Which pathogen causes Dengue fever?

A

Vectors: Aedes aegypti and Aedes albopictus

*Flavavirus, mosquito born disease

81
Q

Where are Aedes mosquitoes found?

A
  • Aedes is common in the southern US, dengue is endemic in northern Mexico, and the US population has no immunity
  • Lack of dengue transmission in the continental US is primarily because contact between people and the vectors is too infrequent to sustain transmission
82
Q

Dengue fever transmission

A
  • The mosquito must feed on a person during a 5-day period when large amounts of virus are in the blood
  • After entering the mosquito in the blood meal, the virus will require an additional 8-12 days incubation
  • The mosquito remains infected for the remainder of its life, which might be days or a few weeks
83
Q

Dengue Fever s/sx

A
  • “Break bone fever”
  • Acute onset of high fever 3-14 days after the bite of infected mosquito
  • Frontal headache
  • Retro-orbital pain
  • Myalgia
  • Arthralgia
  • Hemorrhagic manifestations
  • Rash
  • Anorexia and nausea
84
Q

Complications of dengue fever

A
  • Febrile seizures
  • Dehydration
  • Dengue hemorrhagic fever: severe, fatal form
  • Dengue shock syndrome
85
Q

List the hemorrhagic manifestations

A
  • Skin hemorrhages
  • Epistaxis
  • Gingival bleeding
  • Microscopic hematuria
  • Vaginal bleeding
  • Hematemesis
  • Intracranial bleeding
86
Q

List the s/sx of dengue shock syndrome

A
  • Decrease in level of consciousness
  • Hypothermia
  • Hypoperfusion
  • Metabolic acidosis
  • Progressive organ impairment
  • DIC
87
Q

Diagnosis of dengue fever

A
  • Usually clinical
  • Leukopenia is characteristic, elevated transaminases
  • Thrombocytopenia, fibrinolysis and hemoconcentration- hemorrhagic form
  • Early infection can be confirmed by reverse transcriptase polymerase chain reaction (RT-PCR)
  • A week after, IgM antibodies can be detected
88
Q

Treatment of dengue fever

A
  • No specific therapeutic options besides supportive care.
  • Monitor vitals to assess disease progression
  • Volume support
  • Blood products
  • Vasopressors
  • Acetaminophen: avoid NSAIDs
89
Q

Prevention of Dengue Fever

A
  • Bed nets
  • Repellents
  • Screening blood transfusions
  • Dengvaxia – recombinant, live, attenuated, tetravalent dengue vaccine (CYD-TDV)- 1st vaccine approved, licensed in 6 countries
90
Q

Which pathogen causes yellow fever?

A

Flavivirus infection via Aedes mosquito bite

91
Q

What geographic location is yellow fever found?

A
  • Yellow fever occurs in 47 endemic countries in Africa in Central and South America
  • Around 90% of cases reported every year occur in sub-Saharan Africa
92
Q

S/sx of yellow fever

A
  • May be asymptomatic or have mild symptoms
  • Onset of symptoms typically 3-6 days
  • Sudden onset of fever
  • Chills
  • Severe headache
  • Back pain
  • General body aches
  • Nausea
  • Vomiting
  • Fatigue
  • Weakness
  • Most people with the initial symptoms improve within one week
93
Q

Severe disease sx of yellow fever

A
  • High fever
  • Yellow skin (jaundice)
  • Bleeding
  • Shock
  • Organ failure
  • Severe yellow fever disease can be deadly
  • Among those who develop severe disease, 30-60% die
94
Q

Diagnosis of yellow fever

A
  • Clinical features
  • Serum IgM antibodies
  • Blood samples – virus detection
95
Q

Treatment of yellow fever

A

No treatment or cure- supportive:

  • Rest
  • Fluids
  • Pain relievers- avoid ASA and NSAIDs
  • If severe symptoms, hospitalization may be needed for monitoring
96
Q

What pathogen causes West Nile Virus?

A

West Nile virus is caused by an arbovirus (arthropod borne, RNA viruses)

97
Q

How is West Nile Virus transmitted?

A
  • The virus is carried in the saliva of mosquitoes and is transmitted through bites
  • Birds are the primary hosts (Crow and Cardinals)
  • Infection is spread from bird to bird by mosquitoes
98
Q

Pathogenesis of West Nile Virus

A

Most infected people are asymptomatic unless the infection causes an invasive neurological disease called West Nile Fever

99
Q

S/sx of West Nile Virus

A
  • Fever, headache, myalgia, and anorexia
  • Severe infection can cause profound fatigue, myocarditis, pancreatitis, and hepatitis
  • Particularly severe cases can result in encephalitis or meningitis and death
100
Q

Diagnosis of West Nile Virus

A
  • IgM antibodies – serum or CSF
  • Viral cultures to detect viral RNA(RT-PCR)
  • Immunohistochemistry (IHC) can detect WNV antigen in formalin-fixed tissue
101
Q

Tx of West Nile Virus

A
  • Supportive care
  • No vaccine or specific antiviral available
  • Pain control for headaches and antiemetic therapy and rehydration for associated nausea and vomiting
  • Patients with encephalitis require close monitoring for the development of airway compromise, elevated intracranial pressure and seizures
102
Q

How do humans acquire highly pathogenic avian influenza H5N1?

A

Majority of human H5N1 infection due to direct contact with birds infected with virus**

103
Q

What is H1N1?

A

H1N1 is a swine flu virus is a combination of swine, avian, and human influenza viruses that spreads easily from person to person

104
Q

What population was most affected by H1N1?

A

Higher rate of mortality in the young and middle-age vs elderly for seasonal flu

105
Q

How do humans catch H3N2?

A

H3N2 virus infection sporadically in US states where children and adults have contact with healthy domestic pigs at agricultural fairs

106
Q

S/sx of H1N1 Influenza

A
  • Similar to ordinary influenza, however n/v/d may be more common
  • Mild to sever disease causing pneumonia or respiratory failure
107
Q

Dx of H1N1 influenza

A

Sometimes PCR testing of respiratory samples

108
Q

Tx of H1N1 influenza

A
  • Supportive therapy

- Antivirals for high risk patients

109
Q

Zika virus transmission

A
  • By Aedes mosquitos
  • Local transmission in South America, Central America, Caribbean Islands, Pacific islands, Cape Verde, SE Asia
  • As of October 2016, cases of locally transmitted Zika virus infection has been reported in Miami-Dade County in SE Florida
  • Other modes of transmission: sexual transmission, blood transfusion, organ/tissue transplantation, intrauterine infection
110
Q

S/sx of Zika virus

A
  • Most people are asymptomatic
  • Fever, maculopapular rash, conjunctivitis, joint pain, retro-orbital pain, headache and muscle pain (lasts 4-7 days)
  • Severe infection uncommon; death is rare
  • Zika virus infection during pregnancy can cause microcephaly and other severe fetal brain defects
  • In the US, several cases of microcephaly have been linked to the Zika Virus
111
Q

Dx of Zika virus

A
  • Serologic testing
  • Reverse transcriptase-CR testing
  • Required to notify the CDC if they identify a case of Zika
112
Q

Tx of Zika virus

A
  • Supportive care

- No specific antiviral available

113
Q

Key tasks in dealing with emerging diseases

A
  • Surveillance at national, regional, global level (epidemiological, laboratory, ecological, anthropological)
  • Investigation and early control measures
  • Implement prevention measures (behavioral, political, environmental)
  • Monitoring, evaluation
114
Q

Solutions for emerging diseases - public health surveillance & response systems

A
  • Rapidly detect unusual, unexpected, unexplained disease patterns
  • Track & exchange information in real time
  • Response effort that can quickly become global
  • Contain transmission swiftly & decisively
115
Q

Solutions for emerging diseases - Internet-based information technologies

A
  • Improve disease reporting
  • Facilitate emergency communications &
  • Dissemination of information
116
Q

Solutions for emerging diseases - Human genome project

A

Role of human genetics in disease susceptibility, progression & host response

117
Q

Solutions for emerging diseases - microbial genetics

A
  • Microbial genetics: methods for disease detection, control & prevention
  • Improved diagnostic techniques & new vaccines
  • Geographic Imaging Systems (monitor environmental changes that influence disease emergence & transmission)
118
Q

The best defense (Multi-Factorial)

A
  • Coordinated, well-prepared, well-equipped PH systems
  • Partnerships- clinicians, laboritarians & PH agencies
  • Improved methods for detection & surveillance
  • Effective preventive & therapeutic technologies
  • Strengthened response capacity
  • Political commitment & adequate resources to address underlying socio-economic factors
  • International collaboration & communication

Infectious Disease 2 (13 decks)

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