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
2
Q
Trends since last quarter of 20th century
A
Unusually large number- Rotavirus, Cryptosporidiosis, HIV/AIDS, Hantaviraus, Lyme disease, Legionellosis, Hepatitis C
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
4
Q
Define emerging infectious disease
A
Newly identified & previously unknown infectious agents that cause public health problems either locally or internationally
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
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
7
Q
Factors contributing to emergence
-Environment
A
- Climate & changing ecosystems
- Economic development & Land use (urbanization, deforestation)
- Technology & industry (food processing & handling)
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)
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)
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
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
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
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
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
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
16
Q
Causative organism of anthrax
A
Bacillus anthracis - gram positive, rod-shaped bacteria
17
Q
Where is anthrax found?
A
Found naturally in soil and commonly affects domestic and wild animals around the world
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
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
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
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
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
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
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
25
List the 3 anthrax clinical syndromes
1. Cutaneous
2. Gastrointestinal
3. Inhalational
26
Etiology of the 3 anthrax clinical syndromes
- 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%)
27
How does GI anthrax develop?
After ingestion of contaminated, poorly cooked meat
28
Clinical presentation of GI anthrax
- 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
29
Incubation and fatality of GI anthrax
- Incubation period: 1–7 days
| - Case-fatality: 25–90% (role of early antibiotic treatment is undefined)
30
Clinical presentation of cutaneous anthrax
- 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
31
How does cutaneous anthrax develop?
This form MC encountered in naturally occurring cases*
32
Incubation and fatality of cutaneous anthrax
- Incubation period: 1–12 days
| - Case-fatality: without antibiotic treatment: 20%; with antibiotic treatment: 1%
33
Clinical presentation of inhalational anthrax
- 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.
34
Which symptoms suggest anthrax meningitis?
Confusion, neck stiffness, and headache suggest anthrax meningitis (seen in 50% of patients)
35
What is the incubation period for inhalational anthrax?
1-6 days
36
What symptoms occur during the terminal phase of inhalational anthrax?
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
37
Diagnosis of anthrax
- 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
38
Acute treatment of anthrax
- 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*
39
Post-exposure anthrax treatment
- 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
40
Anthrax Vaccination
- 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.
41
What organism causes the plague?
Yersinia pestis - a Gram negative, nonmotile, nonsporulating bacteria
42
Vector for the plague
- Rodent flea: results in primary bubonic plague
| - The plague bacteria can cycle between rats and their fleas.
43
When was the last plague outbreak?
- 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.
44
Clinical presentation of bubonic plague
- 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
45
Incubation and mortality of bubonic plague
- Incubation 1-8 days (mode 3-5 days)
| - Mortality: Untreated60%; Treated < 5%
46
Pneumonic plague clinical presentation
- 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
47
Which form of plague is the most serious and can be spread person to person?
Pneumonic plague
48
Plague diagnosis
- 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
Plague treatment
| -antibiotic therapy
- 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
Plague - control of secondary transmission
Standard, contact, and aerosol precautions for at least 48 hrs until sputum cultures are negative or pneumonic plague is excluded
51
What is the world's first eradicated disease?
Smallpox
52
When were the last cases of smallpox?
1977- last endemic case in Somalia
1978- two laboratory cases in Britain
1980- WHO declares global eradication of smallpox
53
Which pathogen causes smallpox?
- Variola virus: an Orthopox virus, both minor and major forms of smallpox exist
- Structure is a double stranded, large DNA virus
54
Weaponization of smallpox vs. anthrax
It is not as easily weaponized as anthrax, and requires additional measures to afford the virus the stability in the environment
55
Smallpox prodrome symptoms
- 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
Incubation of smallpox prodrome
Incubation 7-19 days (mean 12)
57
Smallpox clinical presentation
-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
Management of smallpox contacts
-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
Smallpox vaccination
- 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
Complications of smallpox vaccination in normal host
- Inadvertent Autoinoculation (skin, eye)
- Generalized vaccinia
- Erythema multiforme
- Encephalitis
61
Other complications of smallpox vaccination
- Pregnancy: fetal vaccinia
- Dermatoses/Burns: eczema vaccinatum
- Immunocompromised: vaccinia necrosum
62
Smallpox treatment
- Public health emergency
- Supportive care
- Vaccinia Immunoglobulin
- Strict quarantine until scabs off (at least 17 days)
- Cidofovir
63
What kinds of viruses cause Viral Hemorrhagic Fevers (VHFs)?
RNA viruses causing high fevers and generalized vascular damage
64
Which viruses are VHFs?
Filoviruses (Ebola and Marburg)
65
How are viral hemorrhagic fevers spread?
Human infections by insect bites or by contact with blood and body fluids
66
Etiology of VHFs
- 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
VHF pathogenesis
- 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
S/sx of ebola virus
- Fever
- Severe headache
- Muscle pain
- Weakness
- Fatigue
- Diarrhea
- Vomiting
- Abdominal (stomach) pain
- Unexplained hemorrhage (bleeding or bruising)
69
Diagnosis of Ebola virus
- To determine whether Ebola virus infection is a possible diagnosis, there must be a combination of symptoms suggestive of EVD AND a 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
Treatment of Ebola virus
- Supportive
- Oxygen
- Antipyretics
- Antiemetics
- Treat secondary infections if arise
- No antiviral available
71
Which pathogen causes marburg hemorrhagic fever?
Rousettus aegypti - fruit bats are considered to be natural hosts of the Marburg virus
72
Etiology of marburg hemorrhagic fever
- Causes severe viral hemorrhagic fever in humans
- Fatality rates range from 24%- 88%
- No specific antiviral treatment or vaccine is available
73
How is marburg hemorrhagic fever spread?
Virus transmitted to people from fruit bats and spread among humans through human-to-human transmission
74
Prevention of secondary viral hemorrhagic fever transmission
- 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
List the strict barrier precautions (PPE) for VHFs
- Gloves, gown, mask. shoe covers, protective eyeware/faceshield
- Consider HEPA respirator (e.g. N95) for severe hemorrhage, vomiting, diarrhea, cough
76
Prevention of secondary viral hemorrhagic fever transmission cont...
- 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
Diagnosis and tx of VHFs
- 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
How is Dengue transmitted?
Dengue is transmitted primarily from human to human by the bite of the Aedes mosquito
79
Etiology of Dengue fever
- 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
Which pathogen causes Dengue fever?
Vectors: Aedes aegypti and Aedes albopictus
| *Flavavirus, mosquito born disease
81
Where are Aedes mosquitoes found?
- 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
Dengue fever transmission
- 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
Dengue Fever s/sx
- “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
Complications of dengue fever
- Febrile seizures
- Dehydration
- Dengue hemorrhagic fever: severe, fatal form
- Dengue shock syndrome
85
List the hemorrhagic manifestations
- Skin hemorrhages
- Epistaxis
- Gingival bleeding
- Microscopic hematuria
- Vaginal bleeding
- Hematemesis
- Intracranial bleeding
86
List the s/sx of dengue shock syndrome
- Decrease in level of consciousness
- Hypothermia
- Hypoperfusion
- Metabolic acidosis
- Progressive organ impairment
- DIC
87
Diagnosis of dengue fever
- 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
Treatment of dengue fever
- No specific therapeutic options besides supportive care.
- Monitor vitals to assess disease progression
- Volume support
- Blood products
- Vasopressors
- Acetaminophen: avoid NSAIDs
89
Prevention of Dengue Fever
- Bed nets
- Repellents
- Screening blood transfusions
- Dengvaxia -- recombinant, live, attenuated, tetravalent dengue vaccine (CYD-TDV)- 1st vaccine approved, licensed in 6 countries
90
Which pathogen causes yellow fever?
Flavivirus infection via Aedes mosquito bite
91
What geographic location is yellow fever found?
- 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
S/sx of yellow fever
- 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
Severe disease sx of yellow fever
- 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
Diagnosis of yellow fever
- Clinical features
- Serum IgM antibodies
- Blood samples -- virus detection
95
Treatment of yellow fever
No treatment or cure- supportive:
- Rest
- Fluids
- Pain relievers- avoid ASA and NSAIDs
- If severe symptoms, hospitalization may be needed for monitoring
96
What pathogen causes West Nile Virus?
West Nile virus is caused by an arbovirus (arthropod borne, RNA viruses)
97
How is West Nile Virus transmitted?
- 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
Pathogenesis of West Nile Virus
Most infected people are asymptomatic unless the infection causes an invasive neurological disease called West Nile Fever
99
S/sx of West Nile Virus
- 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
Diagnosis of West Nile Virus
- IgM antibodies -- serum or CSF
- Viral cultures to detect viral RNA(RT-PCR)
- Immunohistochemistry (IHC) can detect WNV antigen in formalin-fixed tissue
101
Tx of West Nile Virus
- 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
How do humans acquire highly pathogenic avian influenza H5N1?
Majority of human H5N1 infection due to direct contact with birds infected with virus**
103
What is H1N1?
H1N1 is a swine flu virus is a combination of swine, avian, and human influenza viruses that spreads easily from person to person
104
What population was most affected by H1N1?
Higher rate of mortality in the young and middle-age vs elderly for seasonal flu
105
How do humans catch H3N2?
H3N2 virus infection sporadically in US states where children and adults have contact with healthy domestic pigs at agricultural fairs
106
S/sx of H1N1 Influenza
- Similar to ordinary influenza, however n/v/d may be more common
- Mild to sever disease causing pneumonia or respiratory failure
107
Dx of H1N1 influenza
Sometimes PCR testing of respiratory samples
108
Tx of H1N1 influenza
- Supportive therapy
| - Antivirals for high risk patients
109
Zika virus transmission
- 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
S/sx of Zika virus
* 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
Dx of Zika virus
- Serologic testing
- Reverse transcriptase-CR testing
- Required to notify the CDC if they identify a case of Zika
112
Tx of Zika virus
- Supportive care
| - No specific antiviral available
113
Key tasks in dealing with emerging diseases
- Surveillance at national, regional, global level (epidemiological, laboratory, ecological, anthropological)
- Investigation and early control measures
- Implement prevention measures (behavioral, political, environmental)
- Monitoring, evaluation
114
Solutions for emerging diseases - public health surveillance & response systems
- 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
Solutions for emerging diseases - Internet-based information technologies
- Improve disease reporting
- Facilitate emergency communications &
- Dissemination of information
116
Solutions for emerging diseases - Human genome project
Role of human genetics in disease susceptibility, progression & host response
117
Solutions for emerging diseases - microbial genetics
- 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
The best defense (Multi-Factorial)
- 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
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