Transcript Travel related infections - American College of Physicians

Travel related infections
EMILY WOOD, MD
SEPTEMBER 29, 2013
BAR HARBOR, MAINE
Scope of the issue
 International travel has increased by 50% over the
past decade - 983 million tourist arrivals in 2011
 Long-distance travel, especially to Asia and Africa,
has increased disproportionately
 Travel frequency is also increasing for persons with
comorbid conditions, those traveling for business, or
those visiting friends and relatives
Ann Intern Med. 2013;158:456-468
GeoSentinal data
 Global sentinel surveillance network
 54 globally dispersed physician-based travel/tropical
medicine clinics chosen for experience and training
in travel and tropical medicine
 42,173 ill returned travelers 2007-2011
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GI (34%), fever (23.3%), rash (19.5%)
Asia (32.6%), sub-Saharan Africa (26.7%)
40.5% had pre-travel visit
Ann Intern Med. 2013;158:456-468
Outline of talk
 Fever in returning travelers
 Skin lesions in returning travelers
 Systemic infections
 Local infections
 Diffuse
 Nodular
 Ulcers
 Migratory
 Arthopod
bites
Fever
Malaria
• Protozoan parasite transmitted to human RBCs by
female anophelene mosquito bite
• Plasmodium falciparum and P vivax are most
common
• P vivax and P ovale can persist or stay dormant in
liver as hypnozoites
• P falciparum can result in recrudescence, when
parasites are incompletely eliminated and infection
recurs weeks-months later
Malaria
 3.3 billion people live in areas at risk of malaria
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transmission in 109 countries and territories.
35 countries (30 in sub-Saharan Africa and 5 in Asia)
account for 98% of global malaria deaths.
WHO estimates that in 2008 malaria caused 190 - 311
million clinical episodes, and 708,000 - 1,003,000 deaths.
89% of the malaria deaths worldwide occur in Africa.
Malaria is the 5th cause of death from infectious diseases
worldwide (after respiratory infections, HIV/AIDS,
diarrheal diseases, and tuberculosis).
Malaria is the 2nd leading cause of death from infectious
diseases in Africa, after HIV/AIDS.
Malaria in the US – 2008
• 1,298 reports of cases of malaria with an onset of symptoms in 2008
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among patients in the United States
One transfusion-related case, 1 congenital case, and 2 fatal cases.
Plasmodium falciparum, P. vivax, P. malariae, and P. ovale were
identified in 40.6%, 14.6%, 1.5%, and 1.4% of cases, respectively.
– The first documented case of simian malaria, P. knowlesi, was
reported in a U.S. traveler.
– Eight (0.6%) of the 1,298 patients were infected by two or more
species.
– The infecting species was unreported or undetermined in 41.2% of
cases.
Highest estimated relative case rates among those returning from
West Africa.
A total of 508 U.S. civilians acquired malaria abroad;
– among the 480 civilians for whom chemoprophylaxis information
was known, 344 (71.7%) reported that they had not followed a
chemoprophylactic drug regimen recommended by CDC for the
area to which they had traveled.
MMWR Surveill Summ. 2010 Jun 25;59(7):1-15.
Clinical features
• Patients asymptomatic from time of the original
mosquito bite until approximately a week later
• Typical incubation period usually between 8 – 17
days for P falciparum, P vivax, and P ovale and 18 40 days for P malariae.
• Initial symptoms of malaria are nonspecific and
similar to the symptoms of a minor systemic viral
illness
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fever, headache, fatigue, muscle and joint pain, nausea, and
vomiting
Clinical features
• Classic malaria paroxysm of chills and rigors,
followed by fever spikes, followed by profuse
sweating and fatigue
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Paroxysms coincide with the synchronous rupture of blood
schizonts and liberation of metabolic waste by-products into
the bloodstream.
Can occur in 48-hour cycles (tertian malaria) in P falciparum,
P vivax, and P ovale infections
72-hour cycles (quartan malaria) in P malariae
• Cyclic paroxysms suggestive of malaria but not
always presents, especially early on.
Severe malaria
Clinical Features
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Impaired consciousness/coma
Prostration or sit up with
assistance
Convulsions
Deep breathing, respiratory
distress (acidotic breathing)
Circulatory collapse/shock,
systolic blood pressure <70 mm
Hg
Jaundice
Hemoglobinuria
Abnormal spontaneous bleeding
Acute renal failure
Pulmonary edema (radiologic)
Pathophysiology
• Parasitemia > 5%
• Sequestration of
erythrocytes with mature
forms of the parasite in
deep vascular beds of vital
organs  small infarcts,
capillary leakage, and
organ dysfunction
• Anemia, thrombocytopenia
• 10-20% fatality with
treatment
P falciparum
More likely to cause complicated malaria
P vivax
More likely to cause uncomplicated malaria, can cause more
severe illness
P ovale
More likely to cause uncomplicated malaria
Less likely to cause relapse than P vivax
P malariae
More likely to cause uncomplicated malaria
Very low level of parasitemia
Can have long latency period - up to years
Diagnosis
 Light microscopy – standard tool
 Allows for identification of infection species as well as
quantification of parasitemia
 Should be done every 6-12 hrs for 48 hrs before diagnosis
ruled out
 Drawbacks: labor intensive, time, consuming, requires training
and expertise; less reliable for very low levels of parasitemia
Rapid diagnostic tests
 Introduced in the 1990s
 Use immunochromatographic lateral flow technology for
antigen detection: a blood sample migrates across the
surface of a nitrocellulose membrane by means of capillary
action. The membrane contains stripes of antibodies
specific for different epitopes of a target antigen (one of
which is conjugated to an indicator), along with a control
antibody specific for an indicator-labeled antibody complex
 Antigen targets are malaria antigens conserved across all
human malarias and antigens specific to individual
Plasmodium species
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HRP-2, PLDH, aldolase enzymes
P. falciparum sensitivity and specificity for this test are 95 percent and 94 percent,
respectively; the P. vivax sensitivity and specificity are 69 percent and 100 percent.
Diagnosis and treatment: CDC guidelines
CDC Malaria Hotline: (770) 488-7788 or (855) 856-4713, (770) 488-7100 after hours.
Dengue fever
• Transmitted between people by
mosquitoes Aedes aegypti and A
albopictus.
• Symptoms usually begin 4-7 days after
mosquito bite and last 3 to 10 days
• Rarely transmitted by organ
transplants or blood transfusions, and
there is evidence of vertical
transmission
• Epidemics occur when there is a
concurrence of large number of vector
mosquitoes, a large number of people
with no immunity to 1 of the 4 virus
types (DENV 1-4) and the opportunity
for contact.
• Originated in monkeys and independently jumped to
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humans in Africa or Southeast Asia 100-800 years ago.
Dengue was minor, geographically restricted disease
until the middle of the 20th century.
World War II—in particular the coincidental transport of
Aedes mosquitoes around the world in cargo— thought to
have played a crucial role in the dissemination
First documented in the 1950s during epidemics in
Philippines and Thailand.
1981 - large number of DHF cases began to appear in the
Caribbean and Latin America
Epidemiology
• Over 40% of the world's population at risk from dengue.
• WHO currently estimates may be 50–100 million dengue infections
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worldwide every year.
Before 1970, only nine countries had experienced severe dengue
epidemics.
The disease is now endemic in more than 100 countries in Africa,
the Americas, the Eastern Mediterranean, South-east Asia and the
Western Pacific. The American, South-east Asia and the Western
Pacific regions are the most seriously affected.
Cases across the Americas, South-east Asia and Western Pacific
have exceeded 1.2 million cases in 2008 and over 2.3 million in
2010.
In 2010, 1.6 million cases of dengue were reported in the Americas
alone, of which 49,000 cases were severe dengue.
http://www.who.int/mediacentre/factsheets/fs117/en/index.html
Clinical features
 Incubation 3-14 days
 Majority asymptomatic or fever
plus rash
 Classic dengue: fever, retroorbital headache,
musculoskeletal pain, rash
 Leukopenia, thrombocytopenia
 Diagnosis clinical; also serology,
PCR
Pictures
Dengue Hemorrhagic Fever (DHF)
Dengue Shock Syndrome (DSS)
• Acute immunopathologic
disease that is usually seen in
secondary infection, in 90% of
cases, after exposure to
heterologous DENV serotype
• DHF: fever, positive tourniquet
test, platelets < 100,
hemoconcentration (>20%
above normal)
• Period of defervescence
correlates with onset of
hemorrhagic complications
• DSS: DHF plus shock
Diagnosis
Chikungunya fever
 “Chikungunya”: derived from local language in
Tanzania – “that which bends up” or “stooped walk”
Clinical manifestations – acute
 Abrupt onset fever and malaise after an incubation period of 2-4 days
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(range 1 to 14).
Fever may be high grade (40ºC); usually lasts 3-5 days.
Polyarthralgias begin 2-5 days after onset of fever and commonly
involves multiple joints (often 10 or more joint groups). Joints affected
include hands, wrists, ankles; usually symmetric; distal > proximal
joints.
Skin manifestations seen in 40 to 75 percent of patients – usually
macular or maculopapular rash (appears > 3 days after onset, lasts 3-7
days). Usually on limbs and trunk (and spares the face, palms and soles)
Headache, myalgia, and GI symptoms can be seen.
On physical examination, can see periarticular edema or swelling,
peripheral lymphadenopathy, conjunctivitis may be observed.
Lymphopenia, thrombocytopenia, elevated liver enzymes may be seen.
Clinical manifestations - persistent
• Can have persistent rheumatologic signs and symptoms including
arthritis/arthralgia, edematous polyarthritis of fingers and toes,
morning pain and stiffness and severe tenosynovitis (especially of
wrists, hands and ankles).
• Occasionally, unusual joints (such as sternoclavicular or
temperomandibular joints) involved.
• New onset Raynaud phenomena 2-3 months after infection have been
described in up to 20 percent of cases.
• The duration of persistent symptoms is variable.
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47 patients with acute chikungunya fever followed in Marseilles, France, 82 percent
had persistent joint symptoms. At one, three, and six months following acute illness,
symptoms persisted in 88, 86, and 48 percent of patients, respectively; at 15 months, 4
percent remained symptomatic.
88 patients in Reunion evaluated a mean of 18 months after confirmation of acute
chikungunya infection, 63 percent reported persistent polyarthralgia.
Severe complications
 In older reports, described as a self-limited illness, while severe
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complications and death have been reported in the more recent
outbreaks - ? modulation in virus virulence, improved epidemiologic
observation, or both.
Severe complications and death occur more often among patients
older than 65 years and in those with underlying chronic medical
problems.
Severe complications include respiratory failure, cardiovascular
decompensation, myocarditis, acute hepatitis, renal failure and
neurologic involvement.
Meningoencephalitis is the most common neurologic complication;
can also see acute flaccid paralysis and Guillain Barre syndrome.
In Reunion, the estimated incidence of severe disease was 17 per
100,000 population.
Diagnosis
 Serology is the primary tool for diagnosis in the clinical
setting.
 IgM anti-chikungunya virus antibodies present starting 5
days following onset of symptoms and persist for several
weeks to 3 months.
 IgG antibodies begin to appear about 2 weeks following
onset of symptoms and persist for years.
 In endemic areas chikungunya infection can be suspected
based on characteristic clinical findings in outbreaks
 Viral culture and RT-PCR of Chikungunya virus RNA can
be useful for research purposes.
Treatment
 Supportive care.
 No antiviral agents have been shown to be effective in
human infection
 ribavirin and interferon-alpha appear to have in vitro
activity against virus replication
 ?CHIKV IVIG
 No vaccine is available.
 Patients receiving care in an area inhabited by mosquitoes
competent to transmit chikungunya virus should be treated
in screened, mosquito-free areas or under a bednet to avoid
spread.
JID 2009:200 (15 August)
Chikungunya vs. Dengue
 Chikungunya and dengue virus infections have some
common clinical symptoms and areas of geographic
distribution
 Can be difficult to distinguish in the setting of acute febrile
illness with rash.
 Polyarthralgia occurs in virtually all cases of chikungunya
fever but is not typical of dengue fever (though dengue
fever patients commonly have myalgias).
 Leukopenia, neutropenia and thrombocytopenia
significantly more common in patients diagnosed with
dengue than chikungunya.
Skin lesions in the returning traveler
Surveillance
Am. J. Trop. Med. Hyg., 76(1), 2007,
pp. 184–186
International Journal of Infectious Diseases (2008) 12, 593—602
Rashes in systemic infections: Rickettsial
 Fever, headache, malaise within 1-2 weeks of
infection
 Maculopapular, vesicular, or petechial rash or an
eschar at the site of tick bite
 African tick bite fever
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Southern Africa, tache noir
 Mediterranean spotted fever
 Northern Africa, rash, fever
 Scrub typhus
 Asia, can have lymphadenopathy, cough, hearing
difficulties, and encephalitis
African trypanosomiasis
 Transmitted through bite of tsetse fly
 protozoan parasite Trypanosoma brucei (T. b.
rhodesiense and T. b. gambiense)
 Tsetse flies inhabit rural, densely vegetated areas;
travelers to urban areas are not at risk.
 T. b. rhodesiense: high fever, a chancre at the bite
site, skin rash, headache, myalgia,
thrombocytopenia, and CNS involvement within a
month
 T. b. gambiense: fever, headache, malaise, myalgia,
facial edema, pruritus, lymphadenopathy, and
weight loss, CNS infection in months- years
African trypanosomiasis
PLoS Neglected Tropical Diseases, Nov 2011, Vol. 5 Issue 11, p1-9,
Swimmer’s itch
 Cercarial dermatitis
 Non-human schistosomes
 Distribution of rash is limited
to areas of the body immersed
in water.
 Itchy red papules, may become
vesicular, develop hours to a
day after exposure
 Human schistosomes can also
cause a rash
Seabathers itch
 Salt water exposure
 Jellyfish larvae release
nematocysts, inject toxin
 Distribution matches
areas covered by bathing
suit, etc.
 Inflammatory papules,
can become vesicular or
pustular
Dirofilariasis
 Mediterranean, but
many parts of the world
(US)
 Dog heartworm
 Can be transmitted to
humans by mosquitoes
 Cutaneous or pulmonary
syndrome
Cysticercosis
 Caused by larval state of
pork tapeworm, T. solium.
 Neurocysticercosis versus
extra neural cysticercosis
 Muscle or subcutaneous
infection more common in
patients from Asia, Africa
Leishmaniasis
 Parasitic infection
transmitted by sandfly to
humans and other
mammals
 Many species, vary in
geography, biology, vector
 Three major clinical
syndromes:
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Cutaneous
Mucosal
Visceral
Leishmaniasis
 Endemic in scattered foci
in over 98 countries on 5
continents
 Annual incidence of 0.7 to
1.2 million new cases per
year.
 75% reported from 10
countries: Afghanistan,
Algeria, Brazil, Colombia,
Costa Rica, Ethiopia,
Islamic Republic of Iran,
North Sudan, Peru, and
the Syrian Arab Republic
Herwaldt BL, Stokes SL, Juranek DD. American cutaneous leishmaniasis in US travelers.
Ann Intern Med 1993;118:779–84.
Cutaneous leishmaniasis
 Returning travelers present with nonhealing
cutaneous lesion
 Incubation period of weeks to months
 Papule  nodule  ulceration, often chronic,
slowly progressive
 Nodules, psoriasiform plaques, verrucous lesions,
and sporotrichoid presentations can occur
 Usually painless, rolled edge, can have satellite
lesions
Leishmaniasis
 Diagnosis
 Scraping, aspiration, or biopsy of lesion
 Histology, culture, PCR
 CDC offers diagnostic services
 Treatment
 Many lesions resolve without treatment
 Local versus systemic therapy
Cryotherapy, topical paromycin
 Systemic azoles, miltefosine, sodium stibogluconate,
amphotericin, pentamidine
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Cutaneous larva migrans
 Human infection with non-human hookworms,
usually dog or cat
 Infection most common in tropical and subtropical
countries of Southeast Asia, Africa, South America,
Caribbean, and southeastern United States.
 Larvae found on sandy beaches, in sand boxes, and
under dwellings
 Humans infected when filariform larvae in soil
partially infect skin
 Most frequently on lower
extremities
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buttocks and anogenital
region, trunk, and upper
extremities less often
 Starts as pruritic papule
and develops into
elevated, serpiginous,
reddish-brown lesions in
2-3 days
 10% of cases
vesiculobullous
Strongyloides
 Skin  lungs  small
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intestine
Autoinfection can occur
Eosinophilia
Duodenitis
Cough
Hyperinfection
syndrome
Larva currens – like
CLM, but larva track can
progress 1 cm in 5
minutes
http://www.stanford.edu/group/parasit
es/ParaSites2006/Strongylodiasis/epi
demiology.html
Loaisis
 Parasitic worm, Loa loa, transmitted by deerflies
 Breed in the high-canopied rain forest of West and Central
Africa
 Eye infection
 Calabar swellings
 Worms can survive for > 10 years
Ganthostomiasis
 Asia, Mexico
 Undercooked fish, poultry
 Migrating larvae cause
localized swellings that last
1-2 weeks and associated
with edema, pain, itching,
and erythema
 Swelling can occur for
months-years
 Can migrate throughout
body, including CNS, GI,
GU, lungs, eye
Myiasis
 Maggots of African tumbu fly or South/Central
American botfly
 Eggs hatch and larvae burrow into human skin
 Patients present with persistent boils which exude
serous fluid, can report sensations of movement or
pain in skin
 Close inspection reveals moving spiracles of larvae
Tungiasis
 Tunga penetrans – tiny,
parasitic flea found in W.
Indies, S. and C. America,
W. and E. Africa
 Gravid female burrows into
broken skin on contact and
lives there for 2 weeks until
eggs are ready to be shed.
 Pale/white, annular blisterlike papule with a central
black punctum
Questions or comments?
References
 Centers for Disease Control. Malaria treatment. Available at:
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http://www.cdc.gov/malaria/diagnosis_treatment/treatment.html.
Accessibility verified 9/24/13.
Ansart S, Perez L, et al. Spectrum of dermatoses in 165 travelers returning
from the tropics with skin diseases. Am. J. Trop. Med. Hyg. 2007; 76: 1846.
Leder K, Torresi J, et al. GeoSentinal surveillance of illness in returned
travelers, 2007-2011. Ann Intern Med. 2013: 158:456-468.
Wattal C, Goel N. Infectious disease emergencies in returning travelers.
Med Clin N Am. 2012; 96: 1225-55.
Magill A. Cutaneous leishmaniasis in the returning traveler. Infec Dis Clin
N Am. 2005; 19: 241-66.
Lederman E, Weld L, et al. Dermatologic conditions of the ill returned
traveler: an analysis from the GeoSentinel Surveillance Network. Int J
Infect Dis. 2008; 12: 593-602.
Morris-Jones R, Morris-Jones S. Travel-associated skin disease. Infec Dis
Clin N Am. 2012; 26: 675-89.