See discussions, stats, and author profiles for this publication at: https://www.researchgate.

net/publication/221894813

Scabies in animals and humans: history, evolutionary

perspectives, and modern clinical management

Article  in  Annals of the New York Academy of Sciences · August 2011

DOI: 10.1111/j.1749-6632.2011.06364.x · Source: PubMed

CITATIONS READS

38 5,272

3 authors:

Russell Currier Shelley F Walton

38 PUBLICATIONS   621 CITATIONS    185 PUBLICATIONS   3,323 CITATIONS   

SEE PROFILE SEE PROFILE

Bart J Currie
Menzies School of Health Research
932 PUBLICATIONS   23,179 CITATIONS   

SEE PROFILE

Some of the authors of this publication are also working on these related projects:

Clinical and epidemiological studies of melioidosis View project

Just enjoying my retirement; medical history is my focus. View project

All content following this page was uploaded by Russell Currier on 08 March 2019.

The user has requested enhancement of the downloaded file.

 Ann. N.Y. Acad. Sci. ISSN 0077-8923

A N N A L S O F T H E N E W Y O R K A C A D E M Y O F SC I E N C E S
Issue: The Evolution of Infectious Agents in Relation to Sex

Scabies in animals and humans: history, evolutionary

perspectives, and modern clinical management
Russell W. Currier,1 Shelley F. Walton,2 and Bart J. Currie3
1
American College of Veterinary Medical History Society, Clive, Iowa. 2 Biomedical Science Immunology, University of the
Sunshine Coast, Maroochydore DC, Australia 3 Menzies School of Health Research and Northern Territory Clinical School,
Darwin NT, Australia

Address for correspondence: Russel W. Currier, President, American College of Veterinary Medical History Society, P.O. Box
71003, Clive, IA 50325. ruscurrier@yahoo.com

Scabies, a mite infestation frequently sexually transmitted, dates back to antiquity but remains a challenging parasite
for study in clinical practice and community settings. Its history is one of centuries of slow progress to recognize
the mite and to finally establish its nexus to the clinical syndrome of pruritis with several protean manifestations
and different epidemiological patterns. Contemporary methods of management are briefly reviewed, with the future
promise of improved evolutionary knowledge associated with the advent of molecular and genetic technology. Current
information indicates that humans and earlier protohumans were most likely the source of animal scabies, first of
dogs, and later of other species with subsequent spread to wildlife. Morphologically identical variants of Sarcoptes
scabiei are nonetheless host specific, as determined by recent DNA studies, and invite future investigations into the
dynamics of this troublesome sexually transmissible agent, with the goal of improved recognition and control.

Keywords: scabies; mites; animal hosts; history; evolution

None but kings and princes should have the itch
for the sensation of scratching is so delightful.
— James VI of Scotland and I of England
Introduction
Scabies, from the Latin scabere—to scratch—is a
condition where the skin of an animal or human
host is colonized by the mite Sarcoptes scabiei af-
ter skin-to-skin contact with a donor host. After a
period of time, usually three to six weeks, the in-
festation results in pruritis that remains for an ex-
tended period of time or until treatment of the host.
Demographically in humans, scabies is a common
condition in many developing countries, affecting
large segments of the population, and is also found
worldwide in sexually active young adults and, occa-
sionally, in their children, owing to hands-on care.
A more recent phenomenon is the appearance of
scabies in institutional populations, particularly im-
munosuppressed individuals and in the elderly re-
siding in long-term care facilities. Sarcoptic mange
in animals remains a problem in most areas of the
world.
This paper will review the history and epidemi-
ology of scabies, the developmental stages of the
agent, and the current management of the condi-
tion, followed by a discussion of the paleontological
dynamics of the disease in terms of its evolution and
relationship between humans and animal species.
History
The history of scabies is a long one and was re-
viewed elegantly in several writings by the late Dr.
Reuben Friedman, Temple University in Philadel-
phia, during the first half of the 20th century. He
divided the history in three epochs: “Ancient, Me-
dieval and Modern, or, Pre-Acarian, Acarian, and
Post-Acarian.”1 The ancient period included bib-
lical mention of the term zaraath, which refers
to scabies, and Hebra, a 19th century dermatolo-
gist, found that the term “elephantiasis graecorum”
(leprosy) was likely scabies in many cases, as bathing

doi: 10.1111/j.1749-6632.2011.06364.x
E50 Ann. N.Y. Acad. Sci. 1230 (2012) E50–E60 
c 2012 New York Academy of Sciences.
Currier et al.
in the sulfur-rich River Jordan seven times led
to a cure.2
Greek and Roman investigators, including Aristo-
tle and Galen, appreciated the “contagious” quality
of the condition. Reuben notes that Aristotle was the
“first to have used the term acarus to designate an
animalcule so minute as to be uncuttable or indivis-
ible.” The Roman, Celsus, described sheep scabies
and its treatment—the same as for humans at the
time—with a mixture of sulfur and tar.3
The work of Avenzoar, then in Spain, closes out
this era with his description of the mites, “The little
flesh worms which crawl under the skin of the hands,
legs and feet, and there raise pustules full of water,
are called syrones, asoabat and asoab: so small are
these animals, that they can hardly be seen by the
keenest of vision.”1 But unfortunately, Avenzoar did
not specifically associate the mite with the disease
condition.
During the 13th–16th centuries, a number of
writers observed mites in scabietic lesions, but failed
to make the connection of causality. In the 17th
century, Hauptman produced imperfect drawings
of the mite, followed by Giovanni Cosimo Bonomo,
an Italian naval physician, who with Diacinto Ces-
toni, a pharmacist, studied the condition in sailors
and provided a more accurate drawing of the acarus
mite in 1687, thus discovering and establishing
the parasitic nature of scabies as well as its treat-
ment.4,5 Linnaeus, the Swedish naturalist, classified
the mite in 1746 as Acarus humanus-subcutaneous.6
Finally, the first very accurate illustration of the
mite was drawn by DeGeer, a Swedish naturalist,
whose name remains with the mite nomenclature—
that is, S. scabiei (DeGeer). This acarine period
was closed with the presence and description of
the mite at hand, but the prevailing dogma, how-
ever, precluded acceptance of the cause-and-effect
connection.
A most dramatic incident in the modern history
of scabies occurred on August 13, 1834, when, after
several years of contentious faculty debate, Simon
François Renucci, then a senior medical student in
Paris, obtained a mite from a young female patient
suffering from “the itch.” Renucci accomplished the
task with a technique of removing mites with a nee-
dle probe that he had learned from peasant women
of his native island of Corsica. Success of this proce-
dure depended on not probing the vesicle itself but
slightly off center of the vesicle. Friedman notes this
Ann. N.Y. Acad. Sci. 1230 (2012) E50–E60 
c 2012 New York Academy of Sciences.
Sexually transmitted scabies
“rediscovery” of the mite, 150 years after Bonomo’s
largely forgotten efforts, as representing the begin-
ning of the end of the Galenic era of medicine and
also, by his classification, the end of the Acarian
period of scabies.1,7
The post-Acarian period saw continual advances
through the late 19th and early 20th centuries with
increasing awareness of distinguishing scabies from
other pruritic skin conditions. Ferdinand Ritter von
Hebra in Vienna became the first scientific derma-
tologist with extensive writings on scabies after see-
ing and treating over 40,000 cases. He described the
life cycle and stages of infection and postulated that
species from a variety of animals and humans were
essentially one species.
The persistent misconception at this time was
that the environment remained a means of trans-
mission in some substantial proportion of cases.
Our modern understanding of scabies was enabled
by the extensive work of Kenneth Mellanby, an en-
tomologist in the United Kingdom.8 Mellanby was
commissioned by the United Kingdom to study
scabies from the standpoint of defining measures
for disinfestation of the environment. This need
arose due to major scabies episodes in the United
Kingdom during WW II both in civilians in over-
crowded households and in servicemen. The ur-
gent question needing clarification was to what ex-
tent fomites were a risk to unaffected persons and
how best to decontaminate them. Mellanby initially
studied scabietic soldiers and found that the to-
tal mite burden in most cases was very small—
that is, less than 10, although a few had extensive
mite burdens.8 Subsequently, he secured a facil-
ity to conduct transmission studies using infected
scabietic soldiers and uninfected “volunteers” who
were conscientious objectors during the war. Mel-
lanby’s research showed that fomites—with a few
exceptions—play essentially no role in transmission
for ordinary scabies and that the period necessary
for sensitization was quite long, commonly three
to six weeks. His work stands as a monument to
shattering old myths about the condition and that
human experimentation can be done ethically with
sensitivity as long as the correct arrangements are
set up in advance.9,10 As a final comment, Mel-
lanby’s technique of needle probe removal of mites
is not beyond a clinician’s everyday skills. Interested
readers are referred to J.A. Savin’s comments on
the matter.11
E51
Sexually transmitted scabies Currier et al.

Animal scabies Manfred Green has prepared a valuable summary

of the epidemiology of scabies and noted that inci-
There are six genera of mites found on ani-
dence reached seven to 18 per 1,000 residents in
mals: Cnemidocoptes, Chorioptes, Psoroptes, Notoe-
Europe during epidemics, being reduced to 0.5 to
dres, Otodectes, and Sarcoptes, with only the lat-
2 per 1,000 during nonepidemic periods. Seasonal-
ter addressed in this discussion. Sarcoptic mange
ity is variable with higher incidence in the fall and
has been reported from 10 orders, 27 families, and
winter months. The age distribution is variable also,
104 species of domestic, free-ranging, and wild
but with most cases occurring between the ages of
mammals.12
15–45 years. As noted, sex differences vary a great
For the early work on mange, especially sheep
deal and are influenced by sociocultural factors, in-
scab circa 1800, Hebra cited the works of veterinary
cluding sexual risk patterns within individual coun-
surgeons as being useful, especially those of Walz,13
tries. Institutions may serve as foci for infection,
who linked the condition to mites (sheep scab can be
including hospitals, long-term care facilities, and
caused by Sarcoptes but more commonly Psoroptes
occasionally schools.16
mites). Suffice it to say that the veterinary commu-
Sexual transmission, especially for persons 15–40
nity was ahead of the field of human medicine in
years of age, cannot be overemphasized, but within
recognizing mites as the cause of many scabies-like
households, nonsexual transmission occurs often.
skin conditions, before even Renucci’s “rediscovery”
What stage of the mite actually serves to transfer
of the mite from a human patient. Earlier in 1786,
itself to a new host is a matter of dispute, with
a German physician—Johann Ernst Wichman—
some researchers believing that immature mites fre-
published a monograph on scabies entitled “Aetiolo-
quently wander on the surface of the skin and op-
gie der Krätze,” which provided detailed drawings
portunistically alight on a new host.17 Mellanby
of the mite and included his statement that mange
expressed the view, based on his elaborate stud-
in sheep, same as in humans, is due to mites. Ron-
ies including on his own person, that adult fertil-
calli, in an elegant review of this progress, notes: “In
ized female mites were important in transmission.8,9
1812, Jean Baptiste Gohier (1776–1819 AD), pro-
The life cycle of the mites is presented in Figure 1.
fessor at the (first ever) Veterinary School in Lyons,
In countries with a large proportion of immuno-
France, collected mites from mangy horses, and one
suppressed individuals—for example, HIV patients,
of his colleagues, St. Didier, described and illustrated
the elderly, organ-transplant recipients, and oncol-
them. Dorfeuilles, also from the Veterinary School
ogy patients—the mite burden in some individu-
of Lyons, can also be considered the first scientist
als may be quite high, extending to extraordinary
to have discovered the presence of mites in mangy
numbers as in the rare cases of hyperkeratotic or
cattle.”14 In the ensuing decades and into the 20th
crusted scabies. Nosocomial outbreaks also occur,
century, progress in recognition and management of
with secondary transmission to healthcare workers
animal scabies paralleled that of human medicine.
and tertiary transmission to other patients and to
their household members.18
Epidemiology of scabies in humans
Overview of human clinical scabies:
Scabies pandemics appear at ill-defined secular cy-
recognition and management
cles that persist for about 15 years’ duration with
peak periods in the past century being 1915–1925, Scabies remains one of medicine’s most challeng-
1936–1949, and 1965–1980. Pandemics are associ- ing problems for general practitioners and special-
ated with poverty, poor hygiene, increased sexual ists alike. General groupings of clinical scabies in-
activity, and demographic forces—with wars and clude ordinary scabies commonly seen in healthy
migration being important influences. In developed adults in whom sexual transmission plays a sig-
countries, the longer survival of immunosuppressed nificant role, with subsequent intrafamilial contact
patients has served to expand mite burdens and in- transmission, especially to children. These patients
creased transmission. In the United States, African- have only a small mite burden averaging ∼10 adult
Americans sustain infrequent infections, and overall female mites per patient. At the other extreme is
males outnumber females, although this is not con- the rare crusted or keratotic form of scabies—seen
sistent with experiences in other countries.15,16 frequently in immunosuppressed patients—with

E52 Ann. N.Y. Acad. Sci. 1230 (2012) E50–E60 

c 2012 New York Academy of Sciences.
Currier et al.
Figure 1. Life cycle of Sarcoptes scabiei. With permission from Currie and McCarthy.30
very heavy mite burdens that may number in the
hundreds or thousands, often with little or no pru-
ritis. A third form of scabies is “atypical crusted” sca-
bies cases seen in institutions, nursing homes, and
HIV/AIDS–affected patients who present with an
appreciable mite burden and characteristic pruritis.
A fourth form is the “pseudo- or psycho-scabies”
that is found in successfully treated patients and
institutional employees or family members associ-
ated with known scabies cases, who although not
infested, suffer from delusions as a function of the
“power of suggestion.” This latter group is not to
be confused with the known persistence of inflam-
mation (and itch) that is not uncommon follow-
ing successful therapy in scabies patients and that
can last for several weeks and occasionally longer.
All four forms of scabies present challenges to the
clinician, leading to the observation that “scabies is
Ann. N.Y. Acad. Sci. 1230 (2012) E50–E60 
c 2012 New York Academy of Sciences.
Sexually transmitted scabies
at once the easiest and most difficult diagnosis in
medicine.”
Scabies results from transmission of mites from
an infested patient to an uninfected one after ex-
tensive contact. Adult female mites are fertilized by
males and then burrow into the stratum granulo-
sum of the skin, laying zero to four eggs per day
for up to six weeks before dying. Larvae hatch two
to four days after eggs are laid and cut through the
skin surface and begin to dig new burrows. Three to
four days later, the larvae molt into protonymphs,
which two to three days later molt into tritonymphs,
from which an adult male or female emerges after a
further five to six days. The entire cycle takes about
two weeks (Fig. 1).
After a period of three to six weeks, sensitiza-
tion occurs to mite metabolites, resulting in pruritis.
Sensitization to mite antigens can be demonstrated
E53
Sexually transmitted scabies
a month after following primary infestation, with
both humoral and cellular responses evident.19 Most
importantly these patients can transmit scabies dur-
ing this “incubation period,” leading to the recom-
mendation of treating all members in a household
with some exceptions. Epidemiologic studies sup-
port intrafamilial transmission as being most com-
mon following sexual transmission among adults.9
Clinical features
Scabies in adults and older children usually presents
as an intensely pruritic rash, usually more appar-
ent at night. The rash is considered to result from
combinations of two processes: papular or vesicu-
lar lesions occurring at the site of burrows made
by adult and larval mites and a more generalized
pruritic and erythematous papular eruption that is
unrelated to obvious individual mites and that is
thought to be an immunological response.20 Ar-
eas most frequently affected are where the stratum
corneum is most thin with few hair follicles, com-
monly including the interdigital webs of the digits,
flexor surface of the wrist, extensor surfaces of the
elbows, and other comparable areas but rarely the
face, head, and neck. Children and adults in tropical
regions often have involvement of palms, soles, face,
neck, and scalp.
The classic sign of scabies is the burrow or more
frequently papules. Burrows appear as serpiginous
grayish, reddish, or brownish lines, 2–15 mm long.
Egg cases and mite fecal pellets, or scybala, are
present inside the burrow. The papule at the burrow
surface is usually small and erythematous, often ex-
coriated or covered by a small blood clot. Children
and adults in tropical areas as well as patients who
bathe frequently and practice very good personal
hygiene may not exhibit burrows, thus challenging
clinical suspicion and correct diagnosis.20 Compli-
cating the clinical impression is the fact that affected
skin may exhibit secondary bacterial infection.
Scabies—often compared to syphilis as “the great
imitator”—may exhibit a range of other appear-
ances, including scabies “incognito” in patients who
have received topical or systemic steroids, nodu-
lar scabies with reddish-brown pruritic nodules
present, and rarely crusted or hyperkeratotic scabies,
particularly in patients who are elderly or immuno-
suppressed (Table 1). The crusted scabies patient
in particular has very large mite burdens in their
living environment, clothing, and bedding, posing
E54 Ann. N.Y. Acad. Sci. 1230 (2012) E50–E60 
Currier et al.
Table 1. Differential diagnosis of scabies
Classic scabies
Impetigo, furunculosis
Eczema
Bites (mosquitoes, midges, fleas, lice,
bedbugs, chiggers, other mites)
Tinea corporis
Paronychia
Papular urticaria and other allergic
reactions
Dermatitis herpetiformis
Eczema herpeticum
Crusted scabies
Psoriasis
Skin malignancy (lymphoma, Sezary
syndrome)
Tinea corporis and nail tinea
Syphilis
risk to family and caretakers.21,22 This form of sca-
bies is frequently referred to as “Norwegian” scabies,
as Danielsson and Boeck first described it in Nor-
wegian leprosy patients in 1848.23
Diagnosis and treatment
The diagnosis of scabies is always challenging, lead-
ing to the observation that scabies is “at once the
easiest and most difficult diagnosis in medicine”
(Table 1). Clinically, the presence of burrows is al-
most diagnostic, but as noted earlier, they are not
always present. History of possible or probable ex-
posure and involvement of family members is very
suggestive.24,25 Among techniques for diagnosis is
skin scrapings—exfoliative cytology—in which a
drop of mineral oil or microscopic immersion oil
author R.W.C. preference [Ref. 26] is placed on a
rounded disposable scalpel blade (#10 or 20), and
the suggestive skin lesion is lightly scraped to re-
move the superficial epidermis and the oil deposited
on a microscope slide.26 It is important to remove
material from several lesions onto one slide, and if
sufficient suspect lesions are present, to make at least
four to six slides. Mites, eggs, and scybala should be
examined under low power of 40X in a methodical
manner.27 Note also that one occasionally observes
the very elongated Demodex folliculorum or D. brevis
c 2012 New York Academy of Sciences.
Currier et al.
mites on patients and should not be confused with
“turtle shaped” Sarcoptes mites.
A second technique is to tease out a mite with a
mounted needle probe with the aid of a loupe to
better view the process and suspect location within
a papule or burrow. This area can be better defined
with the burrow ink test, in which a suspect lesion
is rubbed with a blue or black felt tip pen and the
area is then cleansed with an alcohol pad with cap-
illary action, drawing the ink into the tract thereby
forming a characteristic dark, zigzagged line run-
ning across and away from the lesion.28 Lesions can
also be curetted or biopsied if needed.29
Serologic assays are available in veterinary
medicine and are being evaluated for humans but
could be confusing in discriminating current infec-
tions from past exposure. While blood eosiniphilia
and high IgE levels are common in scabies, they are
also seen with many other endemic parasitic infec-
tions.20 Suffice it to say that skin scrapings remain
the “gold standard” of scabies diagnosis and that
needle probe techniques can be employed by clini-
cians who acquire familiarity with the technique in
highly endemic settings.
The mainstay of scabies therapy is topical acari-
cides, although oral ivermectin (extra-label) is in-
creasingly being used in certain circumstances, most
notably for crusted scabies (Table 2). Topical perme-
thrin and oral ivermectin, where affordable, are cur-
rently considered the best treatment options in the
United Kingdom and United States.30–32 As noted in
the table, preventive treatment is also recommended
in close sexual and nonsexual contacts (see evolu-
tionary drug resistance concerns below).
Evolutionary perspectives
Sarcoptes scabiei causes sarcoptic mange in compan-
ion, livestock, and wild animals, as well as scabies
in humans. Infestations often cause significant mor-
bidity and occasional mortality in cases of severe dis-
ease. For many years, host-associated populations of
S. scabiei have been taxonomically divided into mor-
phologically indistinguishable varieties that have a
high degree of host specificity and low degree of
cross-infectivity.33 However, the monospecificity of
these host-specific strains of S. scabiei is controver-
sial, and current studies are investigating whether
they are in fact the same or different species. In the
case of S. scabiei, this is complicated due to many fac-
tors: the indistinguishable morphology of the host-
Ann. N.Y. Acad. Sci. 1230 (2012) E50–E60 
c 2012 New York Academy of Sciences.
Sexually transmitted scabies
associated populations, evidence of apparent cross-
infectivity between hosts demonstrated in emerging
epizootics in sympatric wild animal host popula-
tions,34 limited or no evidence for cross-infestations
occurring between hosts in experimental studies,35
and finally evidence of immunological host-specific
and cross-reactive molecules.36,37
The use of molecular markers has enabled signif-
icant progress to be made in understanding the ge-
netic relatedness of Sarcoptic host-associated popu-
lations, with molecular data providing insight into
both host selection and host-mediated influences on
S. scabiei population structures.38–41 Current indica-
tions suggest that the adaptive evolution of the Sar-
coptes varieties appear to be strongly related to the
phylogenetic similarity of the host species.42 Con-
vincing evidence of limited gene flow was shown
between sympatric populations of human and dog
mites in scabies-endemic indigenous communities
in Australia by Walton and colleagues. These work-
ers were the first to demonstrate, using both nu-
clear and mitochondrial markers, genetically dis-
tinct host-associated populations. The outcomes of
this study were then employed to drive changes
in regional public health policy.38,43 Subsequent to
this work, there have been a number of additional
molecular studies investigating the population dy-
namics and genetic epidemiology of various wild
animal host-associated S. scabiei populations, using
the same multilocus microsatellite markers.34,42,44
These studies provide further evidence that
Sarcoptes is not a single panmictic population and
confirm genetic subdivision according to host with
secondary subclustering related to geographical lo-
cation within host groups. Furthermore, population
structure analysis also revealed temporal stability in
the genetic diversity of Sarcoptes mites.42,45
In regard to evolutionary relationships, molecu-
lar data also suggest that there is substantial evolu-
tionary divergence between human-associated mite
populations and other animal-associated mite pop-
ulations, and that these populations may not have
shared a common ancestor for 2–4 million years.38
However, many evolutionary questions related to
S. scabiei still remain to be answered. When study-
ing closely related parasitic species or populations,
many gene traits are shaped by the demographic his-
tory of the host population and the influence of the
latter on the degree of gene flow and recombination
on the parasite population structure. Introduction
E55
Sexually transmitted scabies Currier et al.

Table 2. Scabies prevention and therapeutic modalities.

Diagnosis Recommended methods Alternative methods Comments

Classic Two applications of topical Two doses of oral ivermectin

scabies permethrin 5% overnight
day 1 and after 1–2 weeks
Crusted Both topical permethrin 5%
scabies every 2 to 3 days for 1 to 2
weeks and oral ivermectin
(200 ␮g/ kg/dose), in three
(days 1, 2, and 8), five (days
1, 2, 8, 9, and 15), or seven
(days 1, 2, 8, 9, 15, 22, and
29) doses, depending on
severity of infectiona
Close A single application of topical
contacts of permethrin 5% applied in
scabies the evening and left on
patients overnight
(200 ␮g/kg/dose) day 1 and
after 1–2 weeks
Topical benzyl benzoate 25% Keratolytic creams for skin
(with or without tea-tree crusts watch; for and treat
oil 5%) instead of secondary bacterial
permethrin infection/sepsis; apply
appropriate measures to
control spread
Oral ivermectin (200
␮g/kg/dose) as a single
dosea

Institutional Treat persons with clinical
outbreak cases as recommended
of scabies above; treat all potentially
exposed residents, staff,
and visitors as
recommended above for
contacts
Endemic Multifaceted approach:
scabies education, community
and com- involvement; treat clinical
munity cases as recommended;
outbreaks treat all family and
household members as
recommended for contacts;
consider treating all other
community members, as
recommended for contact
For refractory outbreaks,
consider treatment of all
residents with oral
ivermectina
Treat persons with classic and
crusted scabies, as well as
contacts in the community,
as recommended above
Look for “core transmitter”
index cases with crusted
scabies; planning and
logistics; measures to
control the spread
Look for “core transmitter”
index cases with crusted
scabies; planning and
logistics of therapy; address
underlying issues of
overcrowding and access to
health hardware (e.g.,
running water), health
care, and education

Adapted with permission from Currie and McCarthy.30

a
Ivermectin is not approved for this indication by the Food and Drug Administration; there are insufficient data on
the safety of ivermectin in pregnancy and in children younger than five years of age.

of scabies mites into naive populations can lead to
founder effects and population substructuring. For
example, there is clear genetic differentiation be-
tween S. scabiei mites obtained from different indi-
viduals of the same host species in the same com-
munity; mites with like genotypes were more often
found within the same host.39 This nonrandom dis-
tribution within individual hosts is characteristic of
other parasite populations, presumably because of
colonization by limited numbers of founders.46–48
Uncertainty in interpretation of phylogenetic re-
lationships in molecular data can also be due to
the different informative values and reliability of
sequences, recombination events, and the possible
persistence of ancestor sequences in populations.
Additional molecular studies investigating the

E56 Ann. N.Y. Acad. Sci. 1230 (2012) E50–E60 

c 2012 New York Academy of Sciences.
Currier et al.
evolutionary relationship of S. scabiei var hominis
with animal-associated populations have not as yet
been published. However, mitochondrial analyses,
restricted to investigations on the phylogenetic lin-
eages of animal associated Sarcoptic mites, showed
limited or no evolutionary substructuring according
to host.49–51 Again the results of these latter studies
may be due to the use of uninformative regions of
mitochondrial DNA, or alternatively evolutionary
relatedness of animal derived Sarcoptes. Although
not validated, the current scientific consensus is
that humans—and protohumans before them—
were the principal host for Sarcoptes mites.1,52
When humans domesticated various species of ani-
mals, of which the dog probably was the first (over
14,000 years ago), behavioral transmission—for ex-
ample, domesticated animals escaping and trans-
mitting to wild animal populations—probably oc-
curred. Recognizing that domestication per se tends
to reduce immunocompetence, domesticated ani-
mals may have been more susceptible to infections,
thereby increasing the probability of mites adapting
to new hosts. Domesticated animals that escaped, in
turn, most likely then infected several wild nondo-
mesticated species.
Phylogenetic relatedness can help to inform so-
lutions to many parasitic diagnostic, treatment, and
epidemiological control problems. The molecular
phylogenetic studies, demonstrating genetically dif-
ferentiated human and animal host-associated mite
populations, reflect attempts at developing serodi-
agnostic tests. Enzyme-linked immunosorbent as-
say (ELISA) kits for serodiagnosis of scabies in ani-
mals, using mite extracts of S. scabiei var. vulpes, are
commercially available.37,53,54 However, these tests
have low sensitivity for human scabies.37 Definitive
diagnosis of scabies infection in humans currently
requires identification of a mite, mite parts, eggs,
or mite fecal pellets in skin scrapings. While this
method is highly specific, the diagnostic sensitiv-
ity is low due to the low number of mites present
in ordinary scabies.55 Currently, a sensitive detec-
tion of IgE reactivity in humans has been developed
with genus-specific scabies mite epitopes for differ-
ential diagnosis of scabies mite allergy from allergy
to house dust mites.56
The spread of the development of resistant mech-
anisms to chemotherapy may also be restricted or
enhanced by Sarcoptes population genetic substruc-
turing. Evidence for de novo ivermectin resistance
Ann. N.Y. Acad. Sci. 1230 (2012) E50–E60 
c 2012 New York Academy of Sciences.
Sexually transmitted scabies
has emerged following intensive therapy of crusted
scabies patients in Darwin, Australia.57,58 Increas-
ing in vitro tolerance of S. scabiei var hominis to
permethrin has also been linked to mutations in
target voltage-sensitive sodium channel genes.59–61
Knowledge of phylogenetic relationships of Sar-
coptes host-associated populations is important, as
possible emerging resistance may arise in sympatric
populations via recombination or horizontal gene
transfer. The existence of a limitation to free gene ex-
change between host-associated populations of sca-
bies mites suggests that effective management prac-
tices can be established for targeted populations.38
Evolutionary studies and population dynamics
may also assist in Sarcoptes vaccine development.
In many developed countries and in some wild an-
imal populations, transmission of the scabies mite
is probably not density dependent, but rather based
more on sexual or familial transmission. If so, the
efficacy of a vaccine may prove debatable. This is in
contrast to disadvantaged communities with high
population densities and endemic scabies, in which
a vaccine would be highly advantageous. However
changing environments such as increasing use of in-
stitutionalized care for the elderly and day care for
the very young, establish susceptible populations
with high population density and reduced immu-
nity. Evidence of increasing institutional outbreaks
of scabies has been reported in the literature.62 Gen-
erally, vaccination is most efficacious in tiny pop-
ulations facing very high infection rates. Design of
future control strategies for scabies will be improved
with increasing information on the epidemiology
and evolutionary relatedness of the Sarcoptes mite
in multiple-host systems, and the vaccination or
treatment protocols likely to be most effective un-
der various conditions.
The inflammatory response to scabies mites may
also have a role in evolution. The severe parasitiza-
tion of the skin in crusted (Norwegian) scabies is
comparable to sarcoptic mange of animals, and it
is not surprising that at one time cases of crusted
scabies were thought to be of animal origin. The
mite burrow is diagnostic for ordinary scabies but
never observed in crusted or animal scabies, and
is similarly not seen on human skin in transient
infestations of animal varieties of scabies mites.
The increased intensity of inflammation in crusted
and animal scabies may reflect changes in host im-
munogenetics, changes in gut microbiota and diet
E57
Sexually transmitted scabies
affecting immunity and/or the effect of cross-
reactivity with other parasites leading to increased
susceptibility and sensitization. Classical transmis-
sion studies document an initial increase in scabies
mite numbers subsequent to primary infestation
with a gradual reduction as host immunity devel-
ops.63 Morgan et al. suggest that the coevolution of
the mite with the mammalian host has favored se-
lection of parasite adaptations, allowing it to down-
regulate aspects of the host’s innate and immune
responses, as seen in ordinary scabies. Experiments
on human skin equivalents demonstrate that sca-
bies mites can downregulate expression of many
cytokines and adhesion molecules of skin epider-
mal keratinocytes, dermal fibroblasts, and dermal
microvascular endothelial cells.64 Further studies
investigating evolutionary relationships may also
help explain differences detected in innate- and
antibody-dependent and independent immune ac-
tivation events in ordinary, crusted, or animal sca-
bies.65 Increased knowledge of the structural and
functional mechanisms of immune evasion and sur-
vival by different host-associated parasite popula-
tions could well lead to improved control and man-
agement.
Concluding remarks
Scabies, as noted in this review, remains a very seri-
ous skin condition in third world settings, institu-
tional populations, and sexually active young adults
with multiple partners and their household mem-
bers. Its continuation dates back to antiquity, ex-
tending back in evolutionary “deep time” as a pos-
tulated uniquely human parasite that expanded its
host base to animals following domestication and
later wildlife species. The evolution of this trouble-
some parasite may be more successfully addressed
with molecular studies of its genetic structure and
immune responses, leading to more effective diag-
nostic capabilities to address the ever-challenging
goals of effective treatment and control.
Conflicts of interest
The authors declare no conflicts of interest.
References
1. Friedman, R. 1934. The Story of scabies. Med. Life 41: 381–
424.
2. Hebra, F.R. 1868. Disease of the Skin, [English translation].
New Sydenham Society, London.
E58 Ann. N.Y. Acad. Sci. 1230 (2012) E50–E60 
Currier et al.
3. Friedman, R. 1934. The Story of scabies – II. Med. Life 1934;
41: 426–476.
4. Warburton, C. 1920. Sarcoptic scabies in man and animals.
Parasitology 12: 265–301.
5. Roncalli, R. 2011. Personal communication.
6. Linnæus, C. 1748. Systema naturæ sistens regna tria natur, in
classes et ordines, genera et species redacta tabulisque æneis
illustrata. 6th Ed., pp. 271. Kiesewetter. Stockholm.
7. Renucci, S.F. 1835. These inaugural sur la decouverte de
l’insecta qui produit la contagion de la gale, du pruigo et du
phlyzacia. Thesis to Paris Faculty of Medicine.
8. Mellanby, K. 1972. Scabies, 2nd ed. E.W. Classey. London.
9. Mellanby, K. 1977. Scabies in 1976. R. Soc. Health J. 97: 32–
40.
10. Mellanby, K. 1973. Human Guinea Pigs. 2nd ed. Merlin Press.
London.
11. Savin, J.A. 2002. Mellanby on scabies. Clin. Exp. Dermatol.
27: 86–87.
12. Pence, D.B. & E. Ueckermann. 2002. Sarcoptic mange in
wildlife. Rev. Sci. Tech. Off. Int. Epiz. 21: 385–398.
13. Walz, G.H. 1809. Natur und Behandlung der Schaaf-Rände.
Stuttgart.
14. Roncalli, R. 1987. History of scabies in veterinary and human
medicine from biblical to modern times. Vet. Parasitol. 25:
193–198.
15. Orkin, M. & H.I. Maibach. 1983. Scabies and pediculosis
pubis. Dermatol. Clin. 1: 111–121.
16. Green, M. 1989. The Epidemiology of Scabies. Epidemiol.
Rev. 11: 126–150.
17. Heilesen, B. 1946. Studies on Acarus scabiei and Sca-
bies. Acta Dermato-Venereologica XXVI(Suppl XIV): 1–
370.
18. Wright, A.J., C. Nassif, V. Miller, et al. 2001. Norwegian
Scabies Causing a Scabies Outbreak In Healthcare Workers
and Patients at a Tertiary Care Medical Center. (Unpublished
oral presentations.) Rochester, Minnesota.
19. Arlian, L.G. 1989. Biology, host relations, and epidemi-
ology of Sarcoptes scabiei. Annu. Rev. Entomol. 34: 139–
161.
20. Currie, B.J. 2005. Scabies. In Tropical Dermatology (Ch 29).
S.K. Tyring, O. Lupi & U. Henggeu, Eds.: 528. Elsevier. Am-
sterdam.
21. Carslaw, R.W., R.M. Dobson, A.J.K. Hood & R.N. Taylor.
1975. Mites in the environment of cases of Norwegian sca-
bies. Br. J. Dermatol. 92: 333–337.
22. O’Donnell, B.F., S. O’Loughlin & F.C. Powell. 1990. Man-
agement of crusted scabies. Int. J. Dermatol. 29: 258–
266.
23. Danielsson, D.C. & W. Boeck. 1848. Traite De La Spedalskhed
Ou Elephantiasis Des Grecs. JB Bailliere. Paris.
24. Orkin, M. 1971. Resurgence of scabies. J. Am. Med. Assoc.
2217: 593–597.
25. Orkin, M. 1975. Today’s scabies. J. Am. Med. Assoc. 233:
882–885.
26. Currier, R.W. & R.I. Ceilley. 2010. Scabies. Human–Animal
Medicine: Clinical Approaches to Zoonoses, Toxicants and
Other Shared Risks. Saunders Elsevier. Maryland Heights,
MO.
27. Orkin, M. & H.I. Maibach. 1983. Scabies and pediculosis
pubis. Dermatol. Clin. 1: 111–121.
c 2012 New York Academy of Sciences.
Currier et al.
28. Woodley, D. & J.H. Surat. 1981. The burrow ink test and the
scabies mite. J. Am. Acad. Dermatol. 4: 715–722.
29. Martin, W.E. & C.E. Wheeler. 1979. Diagnosis of human
scabies by epidermal shave biopsy. J. Am. Acad. Dermatol. 1:
335–337.
30. Currie, B.J. & J.S. McCarthy. 2010. Permethrin and iver-
mectin for scabies. N. Engl. J. Med. 362: 717–725.
31. Orkin, M. & H.I. Maibach. 1993. Scabies therapy—1993.
Semin. Dermatol. 12: 22–25.
32. Lerche, N.W., R.W. Currier, D.D. Juranek, et al. 1983. Atypi-
cal crusted “Norwegian” scabies: report of nosocomial trans-
mission in a community hospital and an approach to control.
CUTIS 31: 637–642.
33. Fain, A. 1978. Epidemiological problems of scabies. Int. J.
Dermatol. 17: 20–30.
34. Alasaad, S., D. Soglia, V. Spalenza, et al. 2009. Is ITS-2 rDNA
suitable marker for genetic characterization of Sarcoptes
mites from different wild animals in different geographic
areas? Vet. Parasitol. 159: 181–185.
35. Arlian, L.G., R.A. Runyan & S.A. Estes. 1984. Cross infes-
tivity of Sarcoptes scabiei. J. Am. Acad. Dermatol. 10: 979–
986.
36. Arlian, L.G., M.S. Morgan & J.J. Arends. 1996. Immunologic
cross-reactivity among various strains of Sarcoptes scabiei. J.
Parasitol. 82: 66–72.
37. Haas, N., B. Wagemann, B. Hermes, et al. 2005. Crossreacting
IgG antibodies against fox mite antigens in human scabies.
Arch. Dermatol. Res. 296: 327–331.
38. Walton, S.F., A. Dougall, S. Pizzutto, et al. 2004. Genetic epi-
demiology of Sarcoptes scabiei (Acari: Sarcoptidae) in north-
ern Australia. Int. J. Parasitol. 34: 839–849.
39. Walton, S.F., J.L. Choy, A. Bonson, et al. 1999. Genetically
distinct dog-derived and human-derived Sarcoptes scabiei
in scabies-endemic communities in northern Australia. Am.
J. Trop. Med. Hyg. 61: 542–547.
40. Alasaad, S., S. Walton, L. Rossi, et al. 2011. Sarcoptes-World
Molecular Network (Sarcoptes-WMN): integrating research
on scabies. Int. J. Infect. Dis. 15: e294–e297.
41. Alasaad, S., R.K. Schuster, F. Gakuya, et al. 2011. Appli-
cability of molecular markers to determine parasitic infec-
tion origins in the animal trade: a case study from Sar-
coptes mites in wildebeest. Forensic Sci. Med. Pathol. Aug 4,
DOI:10.1007/s12024-011-9268-z.
42. Soglia, D., R. Rasero, L. Rossi, et al. 2007. Microsatellites
as markers for comparison among different populations of
Sarcoptes scabiei. Ital. J. Anim. Sci. 6: 214–216.
43. Walton, S., J. Low Choy, A. Bonson, et al. 1999. Genetically
distinct dog-derived and human-derived Sarcoptes scabiei in
scabies-endemic communities in northern Australia. Am. J.
Trop. Med. Hyg. 61: 542–547.
44. Rasero, R., L. Rossi, D. Soglia, et al. 2010. Host taxon-
derived Sarcoptes mite in European wild animals re-
vealed by microsatellite markers. Biol. Conserv. 143: 1269–
1277.
45. Alasaad, S., A. Oleaga, R. Casais, et al. 2011. Temporal sta-
bility in the genetic structure of Sarcoptes scabiei under the
host-taxon law: empirical evidences from wildlife-derived
Sarcoptes mite in Asturias, Spain. Parasites & vectors. [Re-
search Support, Non-U.S. Government]. 4: 151.
Ann. N.Y. Acad. Sci. 1230 (2012) E50–E60 
c 2012 New York Academy of Sciences.
Sexually transmitted scabies
46. Anderson, T.J.C. & J. Jaenike. 1997. Host specificity, evolu-
tionary relationships and macrogeographic differentiation
among Ascaris populations from humans and pigs. Para-
sitology. 115: 325–342.
47. Anderson, T.J.C., M.E. Romero-Abal & J. Jaenike. 1993. Ge-
netic structure and epidemiology of Ascaris populations:
patterns of host affiliation in Guatemala. Parasitology 107:
319–334.
48. Lymbery, A., R. Thompson & R. Hobbs. 1990. Genetic
diversity and genetic differentiation in Echinococcus gran-
ulosus (Batsch, 1786) from domestic and sylvatic hosts
on the mainland of Australia. Parasitology 101: 283–
289.
49. Zahler, M., A. Essig, R. Gothe & H. Rinder. 1999. Molecu-
lar analyses suggest monospecificity of the genus Sarcoptes
(Acari: Sarcoptidae). Int. J. Parasitol. 29: 759–766.
50. Berrilli, F., S. D’Amelio & L. Rossi. 2002. Ribosomal and
mitochondrial DNA sequence variation in Sarcoptes mites
from different hosts and geographical regions. Parasitol. Res.
88: 772–777.
51. Skerratt, L.F., N.J.H. Campbell, A. Murrell, et al. 2002. The
mitochondrial 12S gene is a suitable marker of populations
of Sarcoptes scabiei from wombats, dogs and humans in
Australia. Parasitol. Res. 88: 376–379.
52. Fain, A. 1984. Speciation and evolution in Acari. Acarology
VI 1: 10–18.
53. Hollanders, W., J. Vercruysse, S. Raes & S. Bornstein.
1997. Evaluation of an enzyme-linked immunosorbent assay
(ELISA) for the serological diagnosis of sarcoptic mange in
swine. Vet. Parasitol. 69: 117–123.
54. Curtis, C.F. 2001. Evaluation of a commercially avail-
able enzyme-linked immunosorbent assay for the diag-
nosis of canine sarcoptic mange. Vet. Rec. 148: 238–
239.
55. Walton, S.F. & B.J. Currie. 2007. Problems in diagnosing
scabies, a global disease in human and animal populations.
Clin. Microbiol. Rev. 20: 268–279.
56. Jayaraj, R., B. Hales, L. Viberg, et al. 2011. IgE specificity
for a recombinant allergen of Sarcoptes scabiei: a new di-
agnostic test for scabies. Clin. Microbiol. Infect. 71: 403–
407.
57. Currie, B.J., P. Harumal, M. McKinnon & S.F. Walton.
2004. First documentation of in vivo and in vitro iver-
mectin resistance in Sarcoptes scabiei. Clini. Infec. Dis. 39: 8–
12.
58. Mounsey, K.E., D.C. Holt, J.S. McCarthy, et al. 2009. Lon-
gitudinal evidence of increasing in vitro tolerance of scabies
mites to ivermectin in scabies-endemic communities. Arch.
Dermatol. 145: 840–841.
59. Pasay, C., L. Arlian, M. Morgan, et al. 2008. High-resolution
melt analysis for the detection of a mutation associated with
permethrin resistance in a population of scabies mites. Med.
Vet. Entomol. 22: 82–88.
60. Pasay, C., S. Walton, K. Fischer, et al. 2006. PCR-based assay
to survey for knockdown resistance to pyrethroid acaricides
in human scabies mites (Sarcoptes scabiei var hominis). Am.
J .Trop. Med. Hyg. 74: 649–657.
61. Walton, S.F., M.R. Myerscough & B.J. Currie. 2000. Studies in
vitro on the relative efficacy of current acaricides for Sarcoptes
E59
Sexually transmitted scabies
scabiei var. hominis. Trans.R. Soc. Trop. Med. Hyg. 94: 92–
96.
62. Bouvresse, S. & O. Chosidow. 2010. Scabies in healthcare
settings. Curr. Opin. Infect. Dis. [Review] 23: 111–118.
63. Mellanby, K. 1944. The development of symptoms, parasitic
infection and immunity in human scabies. Parasitology 35:
197–206.
E60 Ann. N.Y. Acad. Sci. 1230 (2012) E50–E60 
View publication stats
Currier et al.
64. Morgan, M.S. & L.G. Arlian. 2010. Response of human skin
equivalents to Sarcoptes scabiei. J. Med. Entomol. 47: 877–
883.
65. Walton, S.F., S. Pizzutto, A. Slender, et al. 2010. Increased
allergic immune response to Sarcoptes scabiei antigens in
crusted versus ordinary scabies. Clin. Vaccine.Immunol. 17:
1428–1438.
c 2012 New York Academy of Sciences.