infectious disease issues in natural disasters

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Infectious Diseases After Natural Disasters Christian Sandrock, MD, MPH California Preparedness Education Network Funded by HRSA Grant T01HP01405

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Infectious Diseases After Natural Disasters

Christian Sandrock, MD, MPH

California Preparedness Education Network

Funded by HRSA Grant T01HP01405

CALIFORNIA PREPAREDNESS EDUCATION NETWORK

A program of the California Area Health Education Centers

calPEN at COMMUNITY HEALTH PARTNERSHIP

• Covers the 9 San Francisco Bay Area counties

• It is a program of the Health Education and Training Center (South Bay AHEC), a division of the Community Health Partnership

• Community Health Partnership is a consortium of community clinics that works to strengthen the healthcare safetynet for the medically underserved

HOUSEKEEPING

• Folder contents

• Sign-in sheet with degree/job function and license number (if applicable)

• Please FILL OUT the participant data form and the evaluation form and TURN IN by the end of the presentation

OBJECTIVES

1. Recognize the risk of infectious diseases after natural disasters

2. Recognize the indications of infectious diseases after natural disasters

3. Meet immediate care needs of patients

4. Alert appropriate authorities

5. Participate in response

Overview

• The role of infectious diseases in natural disasters

• Factors leading to a disease outbreak after a disaster

• Review some of the common and rare diseases after a natural disaster

Background

• Historically, infectious disease epidemics have high mortality

• Disasters have potential for social disruption and death

• Epidemics compounded when infrastructure breaks down

• Can a natural disaster lead to an epidemic of an infectious disease?

• If so, how?

Western K Tropical Public Health, London School of Hygiene and Tropical Public Health

Phases of Disaster

• Impact Phase (0-4 days)– Extrication– Immediate soft tissue infections

• Post impact Phase (4 days- 4 weeks)– Airborne, foodborne, waterborne and vector

diseases

• Recovery phase (after 4 weeks)– Those with long incubation and of chronic

disease, vectorborne

Factors for Disease Transmission After a Disaster

• Environmental considerations

• Endemic organisms

• Population characteristics

• Pre- event structure and public health

• Type and magnitude of the disaster

Environmental Considerations

• Climate– Cold- airborne – Warm- waterborne

• Season (USA)– Winter- influenza– Summer- enterovirus

• Rainfall– El Nino years increase malaria– Drought-malnutrition-disease

• Geography– Isolation from resources

Endemic organisms

• Infectious organisms endemic to a region will be present after the disaster

• Agents not endemic before the event are UNLIKELY to be present after

• Rare disease may be more common

• Deliberate introduction could change this factor

Endemic Organisms

• Northridge Earthquake– Ninefold increase in coccidiomycosis (Valley

fever) from January- March 1994

• Mount St. Helens– Giardiasis outbreak in 1980 after increased

runoff in Red Lodge, Montana from increased ash

Population Characteristics

• Density– Displaced populations– Refugee camps

• Age– Increased elderly or children

• Chronic Disease– Malnutrition– DM, heart disease– transplantation

Population Characteristics

• Education– Less responsive to disaster teams

• Religion– Polio in Nigeria, 2004

• Hygiene– Underlying health education of public

• Trauma– Penetrating, blunt, burns

• Stress

Pre-event resources

• Sanitation• Primary health care and nutrition• Disaster preparedness• Disease surveillance• Equipment and medications• Transportation• Roads• Medical infrastructure

Type of disaster

• Earthquake– Crush and penetrating injuries

• Hurricane (Monsoon, Typhoon) and Flooding– Water contamination, vector borne diseases

• Tornado– Crush

• Volcano– Water contamination, airway diseases

• Magnitude– Bigger can mean more likelihood for epidemics

Howard et al, Emergency Medicine Clinics in North America 1996 14 (2)

Flooding

• Missouri 1993– Increase reports if E.D. visits due to illness– 20% respiratory,17% GI

• Iowa 1993– No reports of GI or respiratory increase due to

sanitation measures

• Florida – Hurricane Andrew– Heavy mosquito spraying lead to no change

in encephalitis rates

Bissell, RA J Emerg Med 1983 1 (1):59-66

Dominican Republic, 1979

• Hurricane David and Fredrick on Aug 31 and Sept 5th 1979

• >2,300 dead immediately• Marked increase in all diseases measured

6 months after the hurricane– Thyphoid fever– Gastroenteritis– Measles– Viral hepatitis

S.F. 1907 Fire Plague Quarantine failure

Duluth, MN 1918

Forest Fire Influenza Crowding, epidemic

Haiti, 1963 Hurricane Malaria Vector control stopped

Italy, 1976 Earthquake Salmonella Carriers

Water sanitation stopped

Epidemics after Disasters

Epidemics after Disasters

Dominican Republic, 1979

Hurricane Thyphoid, GI, hepatitis, measles

Crowding, flooding, chronic disease

Popaya, Colombia 1983

Earthquake Viral hepatitis

Water sanitation

Equador, 1983

Flooding Malaria Vector increase

Summary of Factors

• Many factors play a role in disease development and outbreaks

• Change of disease not likely to play role

• Change and cessation of public health measures play a big role

What infections would we see today?

Endemic organisms

Post-impact phase

Recovery Phase

Post-Impact Phase Infections

• Crush and penetrating trauma– Skin and soft tissue disruption (MRSA)– Muscle/tissue necrosis– Toxin production disease– Burns

• Waterborne– Gastroenteritis– Cholera– Non-cholera dysentery– Hepatitis– Rare diseases

Post-Impact Phase Infections

• Vector borne– Malaria– WNV, other viral encephalitis– Dengue and Yellow fever– Typhus

• Respiratory– Viral– CAP– Rare disease

• Other– Blood transfusions

Recovery Phase Infections

• These agents need a longer incubation period– TB– Schistosomiasis– Lieshmaniasis– Leptospirosis– Nosocomial infections of chronic disease

What effects skin and soft tissue infections?

• Crush and penetrating injuries– ABC’s

• Establish airway• Circulation

– Stabilize• BP support• Respiratory support

– Diagnose extent of injuries• Radiology• Diagnostic procedures

– Corrective action• CT, fracture stabilization, transfusion• Surgery if necessary

What effects skin and soft tissue infections?

• Post-traumatic Care– Hypoxia from pulmonary contusion, ARDS, VAP– Coagulopathy– Renal failure– DVT/PE– Ulcer disease– Soft tissue infections

• Cellulitis • Necrotizing fasciitis• Post op wound infection• Burn care

Cellulitis

• Skin infection involving the subcutaneous tissue

• Predisposing factors– Lymphatic compromise– Site of entry– Obesity– DM– Dirty/contaminated wound

Cellulitis- Microbiology

• Streptococcus• Staphylococcus (MRSA)

– Worse in shelters

• Special circumstances– Water exposure

• Aeromonas (MMWR 2005 Sept;54(38):961 and Clin Infect Dis 2005 Nov;41(10):93)

• Vibrio vulnificus (MMWR 2005 Sept;54(38):961)

• E coli, Klebsiella, Pseudomonas (Lakartidningen 2005 Nov;102(48):3660)

• Myroides, Bergeyella, Sphingomonas• Mucormycosis (Ann Acad Med Singapore 2005)

Cellulitis- Microbiology

• Animal bites– Pasteurella multocida

• DM– Other gram negatives

• Asia– Increased resistance (Lakartidningen 2005 Nov;102(48):3660)

• Leprosy (Emerg Infect Dis 2005 Oct;11(10):1591-3)

• Chemical dermatitis (MMWR 2005 Sept;54(38):961)

Cellulitis

• Pathogenicity– Not well understood– Venous and lymphatic compromise– Bacterial invasion with endo/exotoxin release– Cytokine release

• Symptoms– Systemic- F/C/M– Redness, swelling– Tenderness, edema– May have ulcer or abscess

Cellulitis

• Treatment– Antibiotics (MRSA)

• B-lactam• TMP/SMX• Clindamycin• Linezolid• Vancomycin

– Limb elevation– Systemic support– Surgical consultation

• Abscess• Occular• Necrotizing fasciitis evaluation

Necrotizing Fasciitis

• Fulminant destruction of tissue

• Systemic toxicity

• Very high mortality

• Much larger bacterial load than cellulitis

• Travels through fascial plain

• Much less inflammation from necrosis, vessel thrombosis, and bacterial factors

Necrotizing Fasciitis

• Two types– Type I

• Largely mixed aerobic and anaerobic infection• Seen in post surgical patients• DM, PVD big risk factors• Examples

– Cervical necrotizing fasciitis (Ludwig’s angina)– Fournier’s gangrene

– Type II• Group A strep • Large exotoxin production or M protein• Any age group or without portal of entry

Diagnosis

• Pain– May mimic post surgical changes

• Skin changes– Thick or “woody” in nature– Minimal erythema– Bullae

• Systemic symptoms– Fevers, chills– Rapid sepsis

Treatment

• Surgical Debridement!!!!!!!!– aggressive and explorative– Wide tissue excision

• Antibiotics– B- lactam antibiotics– Clindamycin for toxin production– Gram negative/anaerobic coverage

• Hyperbaric O2• Supportive care

Toxin Diseases

• Tetnus– Rare due to vaccination

– 1 Million die per year in developing world– 4 clinical patterns

• Generalized

• Local

• Cephalic

• Neonatal

Tetanus

• Spores of C. tetani enter the tissue

• Produce metalloprotease, tetanospasmin

• Retrograde movement into CNS

• Blocks neurotransmission by cleaving protein responsible for neuroexocytosis

• Disinhibition of motor cortex

• Extensive spasm

Tetanus

• Needs the right factors to produce– Penetrating injury with spore delivery

– Co-infection with other bacteria– Devitalized tissue– Localized ischemia– Can have water contamination as part of entry

(Ann Acad Med Singapore 2005;34(9):582)

Tetanus Treatment

• Wound management– Halts toxin production

• Tetanus antitoxin and vaccine– Neutralized unbound toxin

• Benzodiazepines and paralytics– Treats spasms

• B-blockers– Treats autonomic dysfunction of late disease

• Supportive care

Waterborne disease

• Viral gastroenteritis– Norovirus (MMWR 2005 Oct;54(40):1016)

• Cholera– Gram negative bacterium Vibrio cholerae

– Severe water diarrhea with 50% mortality if untreated– 190 serrotypes but only O1 and O139 cause human

epidemics– Bacterial model for toxin mediated disease– 2 cases isolated after Katrina with minimal disease

(MMWR Nov 2005)

Cholera pathophysiology

• Enter the small bowel and colonize– Pilus required– Hemagglutanins

– Acessory colonizing factor

– Porin like proteins

• Produces toxin– A with 5 B subunits– A cleaves to A1, activates adenylate cyclase

– Leads to increase Cl secreation and decreased Na absorption

Cholera-symptoms

• Majority are asymptomatic

• Some with develop rapid diarrhea

• Diarrhea most severe days 1-2, stops by day 6

• May loose 100% body weight in 2 days

• Children, elderly at risk

• Death in 2 -48 hours (18 average)

Cholera Treatment

• Oral rehydration- per liter– 3.5g NaCl– 2.9g NaHCO3– 1.5g KCl– 20g glucose

• IV rehydration• Antibiotics- not necessary

– Lessens diarrhea by one day

• Vaccine- no evidence• Public health prevention

Non cholera dysentery

• Giardia• E. Coli• Toxin Mediate food poisoning• Salmonella• Shigella• Campylobacter• Yersinia• Viral hepatitis• Viral Gastroenteritis

Respiratory Illness

• Viral– Most common cause of infectious illness after

Midwest floods over past 20 years– More common is shelter setting (unpublished)

• TB– 25% mortality in camps in Africa and Asia– Worsened by drought

• Community acquired bacterial pneumonia– Mainly theoretical, no data

Recent experiences

• Meliodosis (Emerg Infect Dis 2005 Oct;11(10):1639)

• Necrotizing pneumonia• Multidrug resistant TB (Emerg Infect Dis 2005 Oct;11(10):1591-3)

• Atypical mycobacterial pneumonia (Emerg Infect Dis

2005 Oct;11(10):1591-3)

Vector borne disease

• Malaria– Common after flooding (Prehospital disaster Med 2002;17(3):126)

– Brackish water increases Anopheles (Malar J 2005;4(1):30)

– Well controlled with mosquito abatement

• Encephalitis– No documented increase in US but heavy

abatement programs– West Nile?

General disaster reminders

• Vaccinations are the mainstay of outbreak control in many situations

• Dead bodies pose little to no infectious disease risk (Rev Panam Salud 2004;15(5):297-9)

• Early surveillance and hygiene can stem outbreaks

Conclusions

• Infectious diseases may play a role in the post disaster period

• These diseases will vary depending on many factors

• If the disease if not present before the disaster, it will not be there after

Conclusions

• Early recognition of certain diseases in disaster setting important

• Halting infrastructure and response has led to most increases in infectious diseases

• If deployed, know where you are going and what is endemic

QUESTIONS?

• Please remember to complete:

– Personal data sheet

– Evaluation

– Sign-in sheet (include your degree or job function AND your license number if applicable to receive CEUs)