Emerging Human
Infectious Diseases:
Anthroponoses,
Zoonoses, and
Sapronoses
To the Editor: The source of infection
has always been regarded as an utmost
factor in epidemiology. Human communicable
diseases can be classified according
to the source of infection as anthroponoses
(when the source is an infectious
human; interhuman transfer is typical),
zoonoses (the source is an infectious animal;
interhuman transfer is uncommon),
and sapronoses (the source is an abiotic
substrate, nonliving environment; interhuman
transfer is exceptional). The
source of infection is often the reservoir
or, in ecologic terms, the habitat where
the etiologic agent of the disease normally
thrives, grows, and replicates. A characteristic
feature of most zoonoses and
sapronoses is that once transmitted to
humans, the epidemic chain is usually
aborted, but the clinical course might be
sometimes quite severe, even fatal. An
ecologic rule specifies that an obligatory
parasite should not kill its host to benefit
from the adapted long-term symbiosis,
whereas an occasionally attacked alien
host, such as a human, might be subjected
to a severe disease or even killed rapidly
by the parasite because no evolutionary
adaptation to that host exists (1).
In this letter, only microbial infections
are discussed; metazoan invasion and
infestations have been omitted.
Anthroponoses (Greek “anthrópos” =
man, “nosos” = disease) are diseases
transmissible from human to human.
Examples include rubella, smallpox,
diphtheria, gonorrhea, ringworm
(Trichophyton rubrum), and trichomoniasis.
Zoonoses (Greek “zoon” = animal) are
diseases transmissible from living animals
to humans (2). These diseases were
formerly called anthropozoonoses, and
the diseases transmissible from humans
to animals were called zooanthroponoses.
Unfortunately, many scientists
used these terms in the reverse sense or
indiscriminately, and an expert committee
decided to abandon these two terms
and recommended “zoonoses” as “diseases
and infections which are naturally
transmitted between vertebrate animals
and man” (3). A limited number of
zoonotic agents can cause extensive outbreaks;
many zoonoses, however, attract
the public’s attention because of the high
death rate associated with the infections.
In addition, zoonoses are sometimes contagious
for hospital personnel (e.g., hemorrhagic
fevers). Zoonotic diseases can
be classified according to the ecosystem
in which they circulate. The classification
is either synanthropic zoonoses,
with an urban (domestic) cycle in which
the source of infection are domestic and
synanthropic animals (e.g., urban rabies,
cat scratch disease, and zoonotic ringworm)
or exoanthropic zoonoses, with a
sylvatic (feral and wild) cycle in natural
foci (4) outside human habitats (e.g.,
arboviroses, wildlife rabies, Lyme disease,
and tularemia). However, some
zoonoses can circulate in both urban and
natural cycles (e.g., yellow fever and
Chagas disease). A number of zoonotic
agents are arthropod-borne (5); others
are transmitted by direct contact, alimentary
(foodborne and waterborne), or
aerogenic (airborne) routes; and some
are rodent-borne.
Sapronoses (Greek “sapros” = decaying;
“sapron” means in ecology a decaying
organic substrate) are human diseases
transmissible from abiotic environment
(soil, water, decaying plants, or animal
corpses, excreta, and other substrata).
The ability of the agent to grow
saprophytically and replicate in these
substrata (i.e., not only to survive or contaminate
them secondarily) are the most
important characteristics of a sapronotic
microbe. Sapronotic agents thus carry on
two diverse ways of life: saprophytic (in
an abiotic substrate at ambient temperature)
and parasitic (pathogenic, at the
temperature of a homeotherm vertebrate
host). Typical sapronoses are visceral
mycoses caused by dimorphic fungi
(e.g., coccidioidomycosis and histoplasmosis),
“monomorphic” fungi (e.g.,
aspergillosis and cryptococcosis), certain
superficial mycoses (Microsporum gypseum),
some bacterial diseases (e.g.,
legionellosis), and protozoan (e.g., primary
amebic meningoencephalitis).
Intracellular parasites of animals (viruses,
rickettsiae, and chlamydiae) cannot
be sapronotic agents. The term “sapronosis”
was introduced in epidemiology as a
useful concept (6–8). For these diseases
the expert committee applied the term
“sapro-zoonoses,” defined as “having
both a vertebrate host and a nonanimal
developmental site or reservoir (organic
matter, soil, and plants)” (3,9). However,
the term sapronoses is more appropriate
because animals are not the source of
infection for humans. While anthroponoses
and zoonoses are usually the
domains for professional activities of
human and veterinary microbiologists,
respectively, sapronoses may be the
domain for environmental microbiologists.
The underdiagnosis rate for
sapronoses is probably higher than that
for anthroponoses and zoonoses, and an
increase should be expected in both incidence
and number of sapronoses.
Legionellosis, Pontiac fever, nontuberculous
mycobacterioses, and primary amebic
meningoencephalitis are a few
sapronoses that have emerged in the past
decade. In addition, the number of
opportunistic infections in immunosuppressed
patients has grown markedly;
many of these diseases and some nosocomial
infections are, in fact, also
sapronoses.
As with any classification, grouping
human diseases in epidemiologic categories
according to the source of infection
has certain pitfalls. Some arthropodborne
diseases (urban yellow fever,
dengue, epidemic typhus, tickborne
relapsing fever, epidemic relapsing fever,
and malaria) might be regarded as
anthroponoses rather than zoonoses
because the donor of the infectious blood
for the vector is an infected human and
not a vertebrate animal. However, the
human infection is caused by an (invertebrate)
animal in which the agent replicates,
and the term zoonoses is preferred.
HIV is of simian origin with a sylvatic
cycling among wild primates and accidental
infection of humans who hunted
or ate them; the human disease (AIDS)
might thus have been regarded as a
zoonosis in the very first phase but later
has spread in the human population as a
typical anthroponosis and caused the
present pandemic. Similarly, pandemic
strains of influenza developed through an
antigenic shift from avian influenza A
viruses. For some etiologic agents or
their genotypes, both animals and
humans are concurrent reservoirs (hepatitis
virus E, Norwalk-like calicivirus,
enteropathogenic Escherichia coli,
Pneumocystis, Cryptosporidium, Giardia,
and Cyclospora); these diseases
might conditionally be called anthropozoonoses.
Other difficulties can occur
with classifying diseases caused by
sporulating bacteria (Clostridium and
Bacillus): Their infective spores survive
in the soil or in other substrata for very
long periods, though they are usually produced
after a vegetative growth in the abiotic
environment, which can include animal
carcasses. These diseases should
therefore be called sapronoses. For some
other etiologic agents, both animals and
abiotic environment can be the reservoir
(Listeria, Erysipelothrix, Yersinia pseudotuberculosis,
Burkholderia pseudomallei,
and Rhodococcus equi), and the diseases
might be, in fact, called saprozoonosis
(not sensu 9 ) in that their source can be
either an animal or an abiotic substrate.
For a concise list of anthropo-, zoo-,
and sapronoses, see the online appendix
(available from: URL: http://www.
cdc.gov/ncidod/EID/vol9no3/02-0208-
app.htm.
Zdenek Hubálek*
*Academy of Sciences, Brno, Czech Republic
References
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paradigm. Emerg Infect Dis
1997;3:417–23.
2. Bell JC, Palmer SR, Payne JM. The
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3.World Health Organization. Joint
WHO/FAO expert committee on
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report series no. 169, Geneva; 1959. 3rd
report, WHO Technical Report Series no.
378, Geneva; The Organization; 1967.
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University of Illinois Press; 1966.
5. Beaty BJ, Marquardt WC, editors. The
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University Press of Colorado; 1996.
6. Terskikh VI. Diseases of humans and animals
caused by microbes able to reproduce
in an abiotic environment that represents
their living habitat (in Russian).
Zhurn Mikrobiol Epidemiol Immunobiol
(Moscow) 1958;8:118–22.
7. Somov GP, Litvin VJ. Saprophytism and
parasitism of pathogenic bacteria—ecological
aspects (in Russian). Novosibirsk:
Nauka; 1988.
8. Krauss H, Weber A, Enders B, Schiefer
HG, Slenczka W, Zahner H. Zoonosen, 2.
Aufl. Köln: Deutscher Ärzte-Verlag;
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9. Schwabe CV. Veterinary medicine and
human health. Baltimore: Williams &
Wilkins; 1964.
Address for correspondence: Zdenek Hubálek,
Institute of Vertebrate Biology, Academy of
Sciences, Klásterní 2, CZ-69142 Valtice, Czech
Republic; fax: 420-519352387; e-mail: zhubalek@
brno.cas.cz
Multidrug-