PM2ch36.pdf

Diseases Transmitted Primarily from Animals to Humans

Chapter 36

DISEASES TRANSMITTED PRIMARILY

FROM ANIMALS TO HUMANS

PATRICK W. KELLEY, MD, DRPH

KELLY T. MCKEE, JR., MD, MPH

KENT E. KESTER, MD

WILLIAM R. BYRNE, MD

CLIFTON A. HAWKES, MD

CHRISTIAN F. OCKENHOUSE MD, P H D

ARTHUR M. FRIEDLANDER, MD

LISA A. PEARSE, MD, MPH

JULIE PAVLIN, MD, MPH

COLONEL DAVID HOOVER, MD

LEPTOSPIROSIS

HANTAVIRUSES

TOXOPLAMOSIS

Q FEVER

VIRAL HEMORRHAGIC FEVERS

RABIES

TULAREMIA

ANTHRAX

BRUCELLOSIS

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Military Preventive Medicine: Mobilization and Deployment, Volume 2

P. W. Kelley ; Colonel, Medical Corps, US Army (Retired); Director, Board on Global Health, Institute of Medicine, 500 Fifth Street,

NW, Washington, DC 20001; Formerly, Director, Division of Preventive Medicine, Walter Reed Army Institute of Research, Direc-

tor, DoD Global Emerging Infections System, Silver Spring, MD 20910-7500

K.T. McKee, Jr. , Colonel, Medical Corps US Army (Retired); Director of Extramural Clinical Research, US Army Medical Research

Institute of Infectious Diseases,1425 Porter Street, Fort Detrick, MD 21702; Formerly, Chief, Medical Operations Division, US

Army Medical Research Institute of Infectious Diseases

K.E. Kester , MD, Lieutenant Colonel, Medical Corps, US Army; Chief, Department of Clinical Trials, Division of Communicable

Diseases and Immunology, Walter Reed Army Institute of Research, Silver Spring, MD 20910-7500

W.R. Byrne , MD, Colonel, Medical Corps US Army; Infectious Disease Officer, Infectious Disease Service, Walter Reed Army Medi-

cal Center, Washington, DC 20307-5001; Formerly, Chief, Medical Division, United States Army Medical Research Institute of

Infectious Diseases, Fort Detrick, MD 21702-5011

C.A. Hawkes , MD, Colonel, Medical Corps, US Army; Chief, Infectious Disease Service, Walter Reed Army Medical Center, Wash-

ington, DC 20307-5001

C.F. Ockenhouse MD, PhD, Colonel, Medical Corps, US Army; Infectious Disease Officer, Department of Immunology, Division of

Communicable Diseases and Immunology, Walter Reed Army Institute of Research, Silver Spring, Maryland 20910-7500

A.M. Friedlander , MD, Colonel, Medical Corps, US Army (Retired); Senior Military Scientist, US Army Medical Research Institute

of Infectious Diseases, Fort Detrick, MD 21702-5011; Adjunct Professor of Medicine, Uniformed Services University of the Health

Sciences, 4301 Jones Bridge Road, Bethesda, Maryland 20814-4799

L.A. Pearse , MD, MPH, Major, Medical Corps, US Army; Chief, Mortality Surveillance Division, Armed Forces Institute of Pathol-

ogy, 1413 Research Boulevard, Building 102, Rockville, MD 20850; Formerly, Chief, Preventive Medicine Service, William Beau-

mont Army Medical Center, El Paso, TX 79920-5001

J. Pavlin , MD, MPH, Lieutenant Colonel, Medical Corps, US Army; Chief, Department of Field Studies, Walter Reed Army Institute

of Research, Silver Spring, MD 20910-7500

D. Hoover , MD, Colonel, Medical Corps, US Army; Infectious Disease Officer, Department of Bacterial Diseases, Division of Com-

municable Diseases and Immunology, Walter Reed Army Institute of Research, Silver Spring, MD 20910-7500

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Diseases Transmitted Primarily from Animals to Humans

LEPTOSPIROSIS

Introduction and Military Relevance

Center in Panama, 42% had leptospira in their urine

(Takafuji ET. 1982. Unpublished data). Even dogs

immunized to prevent clinical disease can develop

renal shedding. 4 In the environment, L interrogans

can survive under favorable conditions for as long as

6 months. Tropical, unpolluted, nonsaline, slightly

alkaline waters provide an ideal environment.

Although leptospires usually enter the person

through breaks in skin or mucous membranes, pro-

longed immersion in water may facilitate infection

through otherwise intact skin. Service members

seem to be at particular risk during operations in

swamps, streams, ponds, and muddy areas. Lep-

tospirosis has been particularly noteworthy among

US forces operating in Panama and Vietnam. 1,2

Other professions that are notably at risk include

agriculture and aquaculture, sewer and construc-

tion work, animal husbandry, veterinary and

slaughterhouse work, mining, and laboratory work.

Increasingly, recreational pursuits have been shown

to be correlated with risk; this includes care of pets,

hunting, fishing, swimming in ponds and other

bodies of fresh water, rafting, and playing sports

on muddy fields. 5–7 Other possible routes of infec-

tion implicated include contaminated drinking

water and food preparation surfaces, and, rarely,

animal bites. Extremely rare routes of transmission

include human-to-human transmission through

urine, breast milk, and sex. 8,9

Leptospirosis is a zoonotic infection in which

humans are incidentally infected when they have

direct or indirect skin or mucous membrane con-

tact with the contaminated urine of infected wild

and domestic animals. Leptospirosis has been well

documented in military populations with a history

of exposures to mud or various bodies of water in

endemic locales. 1,2 It is caused by a spirochete, and

transmission can occur in urban, suburban, and

rural settings in both tropical and temperate areas.

The clinical spectrum ranges from an asymptom-

atic or influenza-like infection (the most common

presentation) through hemorrhagic manifestations,

meningismus, jaundice, and renal failure. The more

severe end of the spectrum is called Weil’s syn-

drome. Although efforts at prevention can include

immunization of domestic animals, the major

means of prevention used in the military setting

include education, rodent control, and, when ap-

propriate, weekly doxycycline prophylaxis.

Description of the Pathogen

There are more than 200 antigenically distinct

serovars or strains of leptospire classified into about

23 groups under the species Leptospira interrogans .

The distribution of serovars varies around the

world. The pathogenicity of serovars varies from

animal to animal and even between “identical”

serovars from different regions. 3 A newly recog-

nized species, L fainei , may also affect humans. A

nonpathogenic species, L biflexa , also exists. Ad-

vances in molecular genetics are leading to a vari-

ety of new classification schemes that do not relate

to traditional serological groupings.

Leptospires are obligate aerobes. They are flex-

ible, tightly coiled, helicoidal rods with one or both

ends usually hooked. Due to its thinness and mo-

tility, darkfield microscopy is necessary for optimal

visualization even with staining.

Geographic Distribution

Leptospirosis can be found in almost every coun-

try, though the distribution within a country reflects

the variations in host-animal populations and the

environment. 3 Cases have been recognized in vir-

tually all states in the United States, though most

reports are from Hawaii and the less-arid southern

states. 5

As was clearly evident with US troops training

in Panama, risk may increase significantly in the

rainy season. Rains or flooding can enhance the

flushing of subsurface leptospires into surface wa-

ters and draw shedding rodents and other animals

to swampy areas. 8 Urban flooding following hurri-

canes and other heavy rains is also associated with

increased risk. The seasonality of reported cases

may also reflect the cyclic nature of human agri-

cultural or recreational activity. Though persons

in arid areas tend to be at lesser risk of leptospiro-

sis, significant transmission can occur under the

right environmental conditions, carrier prevalence,

Epidemiology

Transmission

Leptospires can live free or in association with

human and animal hosts. Animals that survive the

acute infection may shed the organisms in their

urine for years. In a 1982 survey of 139 small ani-

mals trapped at the Jungle Operations Training

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Military Preventive Medicine: Mobilization and Deployment, Volume 2

and human behaviors. For example, the concen-

tration of shedding animals and people around

scarce water holes or oases may create opportu-

nities for transmission.

Pathogenesis and Clinical Findings

The underlying pathologic effect of acute lep-

tospirosis resembles a vasculitis with damage to the

endothelial lining of capillaries coupled with

hepatitic and renal tubular dysfunction. 10 Histori-

cally most leptospirosis deaths have been due to

renal failure, but dialysis has reduced the fatality

of this factor. Cardiac effects, to include myocardi-

tis and arrhythmias, are now the leading cause of

death in leptospirosis. Hemorrhagic manifestations

are also common in severe cases. Jaundice is a ma-

jor feature of severe leptospirosis and appears to

reflect hepatic cell dysfunction more than hemoly-

sis. Survivors generally have no lasting liver or re-

nal dysfunction. Repeated infections with other

serovars can occur. Intrauterine infections can cause

fetal loss, premature labor, and congenital infection.

The incubation period for leptospirosis is typi-

cally 7 to 12 days (range: 2 to 26 days). Very short

incubations have been seen in laboratory exposures.

Although about 90% of recognized cases present as

a mild, self-limited febrile illness, in a prospective

serosurvey of soldiers that identified 24 infected

persons, only one denied any symptomatology. 2 It

is quite possible that if all cases were ascertained,

even more than 90% would be recognized as mild.

Mild, anicteric patients often present with the

sudden onset of fever that peaks at 38°C to 40°C.

Other complaints may include headache, chills,

back and joint pain, neck stiffness, and intense

myalgia. Even lightly touching the skin over the

thighs, calves, and lumbosacral muscles may elicit

notable pain. A commonly described finding dur-

Incidence

The incidence of leptospirosis is grossly under-

reported because the clinical presentation is often

that of a nonspecific influenza-like illness. Most

cases are not specifically diagnosed or are misdiag-

nosed as a more common febrile infection such as

dengue. On occasion this can be a fatal mistake.

Clinical awareness of the patient’s epidemiologic

history and a high index of suspicion are essential

to making this diagnosis and instituting timely, ef-

fective therapy.

Leptospirosis occurs both sporatically and in

common-source outbreaks. Probably the highest

incidence documented has been in US forces train-

ing in Panama. Between 1977 and 1982, close surveil-

lance was conducted on seven US Army units at-

tending the 3-week course at the Jungle Operations

Training Center during the fall rainy season. This

surveillance yielded 91 confirmed and probable

cases, for an annualized incidence estimate of 41,000

per 100,000 person years (Takafuji ET. 1984. Unpub-

lished data) (Figure 36-1). Since these troops in

training did not have daily exposure, the real risk

was probably even higher. Clearly these attack rates

indicate that an intense operational exposure to

contaminated environments can have a major impact

on not only individual health but also unit capabil-

ity and mission accomplishment.

Fig. 36-1 . A typical occupational exposure: soldiers in

the mud at the Jungle Operations Training Center,

Panama.

US Army photograph.

Fig. 36-2 . Conjunctival suffusion in a soldier with lep-

tospirosis Photograph: Courtesy of Colonel Ernest

Takafuji, Medical Corps, US Army.

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Diseases Transmitted Primarily from Animals to Humans

ing the first 3 days of illness is conjunctival suffu-

sion, a dilation of the conjunctival vessels without

associated signs of inflammation (Figure 36-2). Gen-

eralized abdominal pain is sometimes noted and

may suggest a “surgical abdomen” or enteric fever.

Nausea, vomiting, diarrhea, and constipation may

also be reported. Skin manifestations of mild lep-

tospirosis can include a variety of rashes, mainly

but not exclusively on the trunk. Meningeal irritation,

photophobia, and a variable degree of physiological

dysfunction may also noted in mild disease.

Although often not noted by clinicians, classi-

cally leptospirosis is described as having an initial

leptospiremic phase followed after a 1- to 5-day

fairly asymptomatic period by a secondary lepto-

spiuric phase. The leptospiremic phase typically

lasts 4 to 7 days and ends about the time antibodies

appear. During the leptospiruric phase, fever re-

turns and may be associated with signs of aseptic

meningitis 10 (Figure 36-3). The severity of the men-

ingitis is variable. The second phase may last 4 to

30 days or longer. In a review of 150 cases in ser-

vice members serving in Vietnam, however, only

48% of cases were noted to have this second phase,

which usually lasted only 1 day. 1

In that minority of cases with severe leptospiro-

sis, the initial fever and generalized abnormalities

can progress to manifest jaundice, azotemia, hem-

orrhage, anemia, shock, and altered mental status.

As the disease progresses into the second week,

hemorrhagic manifestations may be noted in the

skin, conjunctiva, and sputum. 10 Deaths due to adre-

nal hemorrhage have been noted but are rare. Renal

failure, acute respiratory distress syndrome, con-

gestive heart failure, and arrhythmias are additional

manifestations of severe leptospirosis. Hemorrhagic

pneumonitis has been a significant manifestation

in infections acquired in Korea, other Far Eastern

locales, and Nicaragua. Mild proteinuria is a no-

table laboratory finding. Vitamin K can correct the

prothrombin deficiency that is sometimes seen.

Other common laboratory findings include elevated

creatinine phosphokinase and amalyse levels, neu-

trophilia, and thrombocytopenia. During the sec-

ondary phase, the cerebrospinal fluid may show a

pleocytosis. A variety of chest roentgenogram ab-

normalities are common and may include pulmo-

nary opacities, pleural effusion, and evidence of

myositis or pericardial effusion. Electrocardio-

graphic abnormalities are also noted.

Published case fatality rates vary widely, prob-

ably reflecting geographic variation in serovars and

in the low proportion of mild cases that are specifi-

cally diagnosed. Overall, the true case fatality is

ANICTERIC LEPTOSPIROSIS

ICTERIC LEPTOSPIROSIS

(WEIL'S SYNDROME)

First Phase

3–7 days

(Leptospiremic)

Second Phase

0 days – 1 month

(Leptospiruric or Immune)

First Phase

3–7 days

(Leptospiremic)

Second Phase

10 – 30 days

(Leptospiruric or Immune)

Myalgia

Headache

Abdominal Pain

Vomiting

Conjunctival Suffusion

Fever

50+% of cases asymptomatic

Meningitis

Uveitis

Rash

Fever

Jaundice

Hemorrhage

Renal Failure

Myocarditis

Blood

CSF

Urine

Fig. 36-3 . The clinical course of leptospirosis

Reprinted with permission from: Feigin Rd, Anderson DC. Leptospirosis. In: Feigin RD, Cherry JD, eds.

Textbook of Pediatric Infectious Disease . Vol 2. Philadelphia: W.B. Saunders; 1998: 1534.

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