PM2ch38.pdf

Diseases Spread by Close Personal Contact

Chapter 38

DISEASES SPREAD BY CLOSE

PERSONAL CONTACT

GREGORY C. GRAY, MD, MPH; BRIAN FEIGHNER, MD, MPH; DAVID H. TRUMP, MD, MPH;

S. WILLIAM BERG, MD, MPH; MARGAN J. ZAJDOWICZ, MD; AND THADDEUS R. ZAJDOWICZ, MD

RESPIRATORY PATHOGENS

MENINGOCOCCAL DISEASE

TUBERCULOSIS

SEXUALLY TRANSMITTED DISEASES AND HUMAN

IMMUNODEFICIENCY VIRUS INFECTION

VIRAL HEPATITIS

1117

Military Preventive Medicine: Mobilization and Deployment, Volume 2

G.C. Gray, MD, MPH Captain, Medical Corps, US Navy, (Retired); Professor, Department of Epidemiology, University of Iowa

College of Public Health, 200 Hawkins Drive, Iowa City, IA 52242; Formerly, Director, DoD Center for Deployment Health Re-

search, Naval Health Research Center, San Diego, CA 92186-5122

B. Feighner , MD, MPH, Colonel, Medical Corps, US Army; Interim Chair, Department of Military and Emergency Medicine, Uni-

formed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814-4799

D.H. Trump , MD, MPH, Captain, Medical Corps, US Navy; Associate Professor and Director, Medical Student Education Pro-

grams,, Department of Preventive Medicine and Biometrics, Uniformed Services University of the Health Sciences, 4301 Jones

Bridge Road, Bethesda, MD 20814-4799

S.W . Berg , MD, MPH, Captain, Medical Corps, US Navy (Retired); Director, Hampton Health District, 3130 Victoria Boulevard,

Hampton, VA 23661-1588; Formerly, Director for Organizational Development, Navy Environmental Health Center, Norfolk, Vir-

ginia

M.J. Zajdowicz , MD, Captain, Medical Corps, US Navy; Directorate for Medical Affairs, Naval Medical Center, Portsmouth, VA

23708

T. R. Zajdowicz , MD, Captain, Medical Corps, US Navy; Command Surgeon, Joint Task Force Civil Support, US Joint Forces Com-

mand, Fort Monroe, VA 23551

1118

Diseases Spread by Close Personal Contact

RESPIRATORY PATHOGENS

Introduction and Military Relevance

and new military personnel from rural areas were

thought to be at highest risk of developing pneu-

monia. Measles and influenza epidemics were ob-

served to trigger epidemics of S pneumoniae and S

pyogenes infections. 14,15

Senior military officers were determined to re-

duce respiratory disease during the mass mobili-

zation of personnel for World War II. Beginning in

1941, the US Department of War established the

Board for the Investigation and Control of Influenza

and Other Epidemic Diseases in the Army. Later,

this board assembled various commissions of sci-

entific experts and established numerous public

health and research facilities to study and prevent

respiratory disease. 16 These joint military and uni-

versity endeavors led to many of the antibiotic and

vaccine prophylaxis interventions now used in mili-

tary populations (Table 38-1).

As a result of these and subsequent research ef-

forts, today most US military personnel receive

enzathine penicillin (BPG) or oral erythromycin

rophylaxis, adenovirus vaccines (when available),

uberculosis screening, and influenza vaccine duri-

ng their first military training. This is followed by

nnual influenza vaccination and periodic tubercul-

osis screening throughout their military careers.

he pathogens recognized to cause respiratory dise-

ase among these young adults are similar to those

ausing community-acquired disease among the

eneral US adult population. 17–20 Most frequently,

he pathogens include S pyogenes , Mycoplasma

neumoniae, S pneumoniae, Chlamydia pneumoniae ,

denoviruses, influenza viruses, and rhinoviruses.

ess frequently, military personnel also suffer inf-

ections from Haemophilus influenzae , H parainfluenzae,

egionella pneumophila , Moraxella catarrhalis, Bordetella

ertussis, coxsackieviruses, respiratory syncytial

irus, and parainfluenza viruses. The most signifi-

cant pathogens to military populations are reviewed

here in more detail.

Respiratory pathogens have plagued military

populations throughout US history. Records from

the War of 1812, the Spanish American War, and

World War I document the devastation respiratory

pathogens have caused and the inability of public

health officials to control them. 1–3 Especially well

documented are the epidemics that occurred dur-

ing the mobilization for World War I. In 1918, a 30-

day epidemic of Streptococcus pneumoniae infections

occurred at a military camp in Illinois, causing 2,349

hospital admissions for pneumonia and a 50% mor-

tality rate. 4 During 1918, a 2-month military epi-

demic of influenza in Little Rock, Arkansas, affected

12,393 men and led to 1,499 cases of pneumonia,

31% of whom died during treatment. 5 Other reports

record that hemolytic streptococci ( Streptococcus

pyogenes ) were a continual cause of military epidem-

ics of bronchopneumonia, empyema, and pharyn-

gitis. In total, it was estimated that more than 1.4

million US Army personnel suffered from respira-

tory disease during World War I, accounting for

more than 41% of all forms of disease and causing

more than 77% (45,000) of Army disease deaths. 2

Before antimicrobials were widely available,

strategies to prevent military epidemics of respira-

tory disease were not very successful. Generally,

military public health officers could do little more

than attempt to isolate and treat the afflicted with

various therapies against streptococci, which in-

cluded digitalis, whiskey, strychnine, and various

horse sera. 6–8 Following the success of researchers

in South Africa, US military officials attempted to

control S pneumoniae epidemics at select US Army

camps during World War I with a crude vaccine, 9,10

but their efforts were unsuccessful. 3,11 Commenting

on the trade-off between isolating the ill and com-

promising the mission, one military physician of

1917 wrote that “Exposure to infection and hard-

ships which will result in deaths from pneumonia

may be just as necessary as going into action with

resulting deaths from gunshot wounds.” 7

Despite the limited effective interventions avail-

able to public health officials in the preantibiotic

era, they made important observations regarding

the types of acute respiratory diseases and their

apparent bacterial causes. Those officials noted that

crowding greatly contributed to respiratory epi-

demics 12,13 and that more important than reduced

floor space in sleeping quarters was the number of

men placed in the same room. 13 Southerners, blacks,

Streptococcus pyogenes

S pyogenes is a leading cause of bacterial respira-

tory morbidity among US military personnel. New

military trainees are at particularly high risk of clini-

cally significant infection. During the late 1940s and

the 1950s, dedicated scientific teams, sponsored by

Army Board Commissions, worked at a number of

Army, Navy, Air Force, and Marine Corps training

centers and made much progress in understanding

and controlling this pathogen.

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Military Preventive Medicine: Mobilization and Deployment, Volume 2

TABLE 38-1

IMPORTANT EVENTS IN THE DEVELOPMENT OF MILITARY STRATEGIES TO PREVENT

EPIDEMICS OF ACUTE RESPIRATORY DISEASE

Event

Year Reference

Streptococcus pneumoniae vaccine is effective in South Africa

1911 Maynard a

First US Army troops receive an S pneumoniae vaccine—not effective

1918 Cecil b

Influenza virus discovered

1933 Smith c

First influenza vaccine with protective results

1936 Chenoweth d

Daily oral sulfonamide therapy found to prevent recurrences of rheumatic fever among

1939 Coborn e

civilian populations

US Navy administers oral sulfonamide therapy as mass prophylaxis with good success to eight

1944 Coborn f,g

large training stations that have high S pyogenes disease rates, but therapy-induced sulfa

resistance among endemic S pyogenes strains

Eaton agent is identified (later it is called Mycoplasma pneumoniae ) and is found to cause much

1944 Eaton, h

respiratory morbidity among military trainees

Chanock i

First US Navy personnel receive S pyogenes vaccines—ineffective

1944 EUNo-22 j

Oral penicillin therapy found to prevent rheumatic fever in civilian populations

1948 Milzer k

Procaine penicillin G injection therapy found to prevent rheumatic fever in military personnel

1950 Denny l

with S pyogenes pharyngitis

Oral penicillin first used in US military personnel with excellent prophylaxis success against

1951 NMRU–4 m

S pyogenes

Benzathine penicillin G first used among civilian populations to prevent S pyogenes infection

1951 Stollerman n

Adenovirus discovered and later found to cause much respiratory morbidity among military

1954 Hilleman, o

trainees

Davenport p

Benzathine penicillin G used prophylactically against S pyogenes among large populations of

1956 Frank q

US military personnel

Inactivated adenovirus vaccine (types 4 and 7) found effective among US military trainees

1956 Hilleman r

A new chlamydial pathogen is recognized (later called Chlamydia pneumoniae ) and found to cause

1965 Grayston, s

epidemics of respiratory morbidity among military trainees

Kleemola t

Oral adenovirus vaccines (types 4 and 7) found effective among military trainees

1971 Gaydos u

Long absent, acute rheumatic fever epidemics recur among US military personnel

1987 Wallace v

a. Maynard GD. An Enquiry into the Etiology, Manifestations, and Prevention of Pneumonia Amongst Natives on the Rand, Recruited from Tropical Areas .

Johannesburg, South Africa: South African Institute for Medical Research; 1913: 62–91.

b. Cecil RL, Austin JH. Results of prophylactic inoculation against pneumococcus in 12,519 men. J Exp Med. 1918;28:19–41.

c. Smith W, Andrewes CH, Laidlaw PP. A virus obtained from influenza patients. Lancet . 1933;2:66–68.

d. Chenoweth A, Waltz AD, Stokes J Jr, et al. Active immunization with the viruses of human and swine influenza Am J Dis Child. 1936;52:757-758.

e. Coborn AF, Moore LV. The prophylactic use of sulfonamide in streptococcal respiratory infections, with especial reference to rheumatic fever.

J Clin Invest. 1939;18:147–155.

f. Coborn AF. Mass chemoprophylaxis: The U.S. Navy’s six months’ program for the control of streptococcal infections. Naval Med Bull. 1944;284:149–162.

g. Coburn AF. The prevention of respiratory tract bacterial infections by sulfadiazine prophylaxis in the United States Navy. JAMA. 1944;126:88–93.

h. Eaton MD, Meiklejohn G, Van Herick W. Studies on the etiology of primary atypical pneumonia: A filterable agent transmissible to cotton rats,

hamsters, and chick embryos. J Exp Med. 1944;79:649–668.

i. Chanock RM, Fox HH, James WD. Epidemiology of M. pneumoniae infection in military recruits. Ann N Y Acad Sci. 1967;143:484–496.

j. Epidemiology Unit No. 22. Failure of type specific Streptococcus pyogenes vaccine to prevent respiratory infections Naval Med Bull. 1946;46:709–718.

k. Milzer A, Kohn KH, MacLean H. Oral prophylaxis of rheumatic fever with penicillin. JAMA. 1948;136:536–538.

l. Denny FW, Wannamaker LW, Brink WR, Rammelkamp CH Jr, Custer EA. Prevention of rheumatic fever: treatment of the preceding streptococcal

infection. JAMA 1950;143:151–153.

m.The Personnel of Naval Medical Research Unit No. 4. The Prophylaxis of Acute Respiratory Infections With Oral Penicillin or Chlortetracycline: Antibi-

otics Annual, 1953–54 . New York: Medical Encyclopedia, Inc; 1954: 123–136.

n. Stollerman GH, Rusoff JH. Prophylaxis against group A streptococcal infections in rheumatic fever patients: Use of new repository penicillin

preparations. JAMA. 1952;150:1571–1575.

o. Hilleman MR, Werner JH. Recovery of new agent from patients with acute respiratory illness. Proc Soc Exp Biol Med. 1954;85:183–188.

p. Davenport FM. Influenza viruses. In: Evans AS, ed. Viral Infections in Humans . New York: Plenum Publishing Corp; 1984: 373–396.

q. Frank PF. Streptococcal prophylaxis in Navy recruits with oral and benzathine penicillin. U.S. Armed Forces Med J. 1958;4:543–560.

r. Hilleman MR. Efficacy of and indications for use of adenovirus vaccine. Am J Public Health. 1958;48:153–158.

s. Grayston JT, Woolridge RL, Wang SP, et al. Field studies of protection from infection by experimental trachoma virus vaccine in preschool-aged

children on Taiwan. Proc Soc Exp Biol Med. 1963;112:589–595.

t. Kleemola M, Saikku P, Visakorpi R, Wang SP, Grayston JT. Epidemics of pneumonia caused by TWAR, a new chlamydia organism, in military

trainees in Finland. J Infect Dis . 1988;157:230–236.

u. Gaydos CA, Gaydos JC. Adenovirus vaccines in the U.S. military. Mil Med. 1995;160:300–304.

v. Wallace MR, Garst PD, Papadimos TJ, Oldfield EC. The return of acute rheumatic fever in young adults. JAMA . 1989;262:2557–2561.

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Diseases Spread by Close Personal Contact

Description of the Pathogen

pyrogenic exotoxins A and B and other virulence

factors have been implicated in severe infection.

Numerous theories regarding the interaction of host

immune response and S pyogenes virulence factors

have been postulated; however, it remains unclear

why one person is severely infected by a particular

strain of S pyogenes and another person is merely

colonized with the same S pyogenes strain and suf-

fers no symptoms.

S pyogenes , unlike other β-hemolytic streptococci,

is implicated as a cause of numerous acute clinical

manifestations, such as pharyngitis, peritonsillar

abscess, pneumonia, empyema, scarlet fever, necro-

tizing fasciitis, myositis, bacteremia, and strepto-

coccal toxic shock syndrome. S pyogenes also causes

the nonsuppurative manifestations of acute rheu-

matic fever and glomerulonephritis. The severity

of S pyogenes infections has changed over time. In

the late 1800s, epidemics of scarlet fever were com-

mon and associated with high mortality rates. 25

To day, epidemics of scarlet fever are relatively

rare. 26 In a similar fashion, acute rheumatic fever

was very common during the mobilization for

World War II, with 21,000 cases recorded in the US

Navy alone, 27 but, until the 1980s, few cases were

detected among military populations. 28,29 Changes

in disease rates have been attributed to changes in

the prevalence of virulent strains of S pyogenes . 30

S pyogenes is a Gram-positive coccus, or spherical

bacteria, which, when grown on sheep blood agar,

causes a clear zone of complete hemolysis (β-hemoly-

sis). It is distinguished from other β-hemolytic

streptococci by physiological and immunologic

characteristics and by its implication as a cause of

numerous acute clinical manifestations. S pyogenes

strains are classified according to their capsular

proteins, specifically T and M proteins. More than

90 unique M protein types have been identified. M

types 1, 3, and 18 are associated with acute rheu-

matic fever, and M types 1, 3, 4, 12, and 25 are often

associated with glomerulonephritis.

Epidemiology

The epidemiology of S pyogenes infection has

been well described in military populations. Stud-

ies by military and university investigators in the

1950s demonstrate that transmission is most often

by direct contact or large respiratory droplets and

not commonly by fomites. The bacteria are thought

to be endemic throughout the world, with perhaps

some variation in the endemnicity of certain strains.

Without prophylaxis, recent serologic evidence

demonstrates that as many as 24% of military train-

ees may be infected over an 11-week period. 21

Risk factors for serologic evidence of S pyogenes

infection include being new to the military, crowd-

ing, lack of prophylaxis, close contact with an S

pyogenes carrier, and close contact with a trainee not

on prophylaxis. 22 A retrospective study of civilians

with invasive S pyogenes infections suggested that

Native Americans, and persons older than 65 years

may be at higher risk of severe S pyogenes disease. 23

Active surveillance among Canadians have dem-

onstrated that infection with human immunodefi-

ciency virus, cancer, diabetes, alcohol abuse, and

chickenpox are risk factors for invasive S. pyogenes

disease. 24

Diagnostic Approaches

Even in high-prevalence situations such as epi-

demics, it is difficult to clinically distinguish S

pyogenes pharyngitis from pharyngitis caused by

other pathogens. Diagnosis is best made by culture

or rapid antigen detection. Generally, a rapid anti-

gen test is accepted if it is positive, but it should be

confirmed by culture if it is negative. Because a high

proportion of infected military persons may not

seek medical attention despite symptoms, epide-

miologic studies of S pyogenes generally are con-

ducted by relying on serologic tests, particularly the

antistreptolysin O test. A two-dilution rise in anti-

streptolysin O titer is considered evidence of infec-

tion. Generally, such a rise may be detected in

paired sera drawn 2 to 3 weeks apart. Other sero-

logic tests for S pyogenes infection include the

antideoxyribonuclease B test, the antihyaluronidase

test, and a hemagglutination test (Streptozyme).

Some patients with glomerulonephritis or symp-

toms of acute rheumatic fever may not demonstrate

a rise in antistreptolysin O titer and should be evalu-

ated further with antideoxyribonuclease B or

antihyaluronidase tests before S pyogenes is elimi-

nated as a cause.

Pathogenesis and Clinical Findings

S pyogenes colonizes respiratory mucosal cells,

causing pharyngitis and other clinical manifesta-

tions, such as fever and leukocytosis, in 36 to 72

hours. The complex interaction of cellular and extra-

cellular S pyogenes products with the host immune

system is not well understood, but it is recognized

that immunity to S pyogenes is type-specific. Some

patients progress to more invasive forms of infec-

tion, including streptococcal toxic shock syndrome,

bacteremia, and necrotizing fasciitis. S pyogenes

1121

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