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143
10.9 Treatment
Penicillin is the only drug with proven efcacy in treating CS and the only treatment
option with a low side-effect prole [12, 23, 49]. There is insufcient data on the
efcacy of non-penicillin drugs. Thus, the AAP and CDC insist on penicillin therapy after desensitization in infants with penicillin allergy [12, 27]. The same diagnostic and treatment algorithm should be applied to syphilitic infants born to
HIV-infected mothers [50].
Two different 10-day course penicillin options exist in the treatment of CS: intravenous (IV) aqueous penicillin G (50,000units/kg, q12h [every 12h] in infants
≤1week old, q8h [every 8h] in infants >1-week to ≤4-week old, and q6h [every
6h] in infants >4-week old)×10days, or IM procaine penicillin G (50,000units/kg
as a single daily dose for 10days). Although the CSF penicillin levels are lower
when applied in IM procaine penicillin G form than IV aqueous penicillin G, no
treatment failures have been reported, and the clinical signicance is unknown
[12, 51].
The single-dose regimen (penicillin G benzathine, 50,000 units/kg, IM) is
strongly discouraged in infants of inadequately treated mothers unless the newborn
undergoes a complete evaluation and is found to be normal [12, 50]. In addition,
CNS involvement should undoubtedly be excluded since it requires a 10-day
regimen.
For infants >1month of age, either the late diagnosis of early CS, late CS, or
acquired syphilis, aqueous penicillin G (50,000 units/kg, IV, q4–6h for 10 days)
treatment is recommended. In the presence of CNS involvement, some experts recommend an additional single dose of penicillin G benzathine (50,000units/kg, IM)
before the 10-day aqueous penicillin G course [23].
In the early course of the treatment (most commonly in between 2 and 12h), an
adverse reaction with penicillin, the so-called Jarisch-Herxheimer reaction, may
occur. Endotoxin-like compounds released from the fragmented T. pallidum are
thought to cause this reaction. Jarisch-Herxheimer reaction consists of fever, headache, and myalgia, although hypotension, tachycardia, and tachypnea can occur in
some cases [23, 52].
10.10 Follow-Up andOutcome
For long-term follow-up, infants with CS and all serologically reactive infants
should be evaluated with a thorough clinical and serologic examination via NTTs
(VDRL or RPR) every 2–3 months until they are non-reactive [29]. A hearing
screen, ophthalmologic examination, and the evaluation of neurodevelopmental
progress should be performed yearly [3]. Maternal-origin NTTs usually become
negative within 3months, and if the child is not infected, they should be negative at
6months [15]. The response may be slower in infants and children treated after the
neonatal period [23]. Positivity of the maternal origin TTs may persist beyond
12–15months of age in a proportion of uninfected children. Thus they have limited
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E. M. Kara et al.
value in the follow-up. However, a positive TT titer in a child older than 18months
indicates CS [3].
After ages 6–12months, in cases where NTT titers do not decrease or, on the
contrary, increase, patients should be completely reevaluated and treated with a
10-day course of penicillin, whether or not they had been treated before. A complete
reevaluation should include CSF analysis (for VDRL, cell count, and protein), complete blood and liver function tests, hearing and ophthalmologic examinations, and
long bone radiographs as clinically indicated [15, 23, 37]. In the past, serial CSF
examinations were recommended to be performed every 6months in children with
initially abnormal CSF results; however, recent recommendations [12, 27] state that
serial examinations may be deferred in patients who do not exhibit signs of progressive disease and have normalization of their NNT [42]. Nevertheless, detailed neuroimaging may be warranted in children with persistent CSF abnormality [23].
Congenital syphilis has a 6–8% case fatality rate among infants of mothers with
non or inadequate prenatal care [23, 53]. Proper treatment within the rst 3months
of life may prevent late complications of early CS, although some of them, like
interstitial keratitis and “saber shins,” may persist despite therapy [15, 23]. Osseous
lesions heal over time regardless of treatment [23].
10.11 Prevention
In prevention, screening pregnant women and international adoptees, contact tracing, and long-term follow-up of CS cases with appropriate treatment are essential [23].
10.12 Conclusion
Congenital syphilis is a preventable and treatable infectious disease insidious global
health problem. Besides several clinical manifestations, bilateral, sudden sensorineural HL may occur in the late form of the disease. However, the literature data on
HL related to CS is limited. Penicillin is the drug of choice for the treatment of
CS.Infants with CS require long-term follow-up and may experience late manifestations despite appropriate therapy.
References
1. Korenromp EL, Rowley J, Alonso M, etal. Global burden of maternal and congenital syphilis
and associated adverse birth outcomes—estimates for 2016 and progress since 2012. PLoS
One. 2019;14:e0211720. [correction: PLoS One 2019;14:e219613].
2. Dobson SR.Congenital syphilis: clinical features and diagnosis. In: Kaplan SL, Weisman LE,
editors. UpToDate. Waltham: UpToDate (updated: Mar 26, 2021; literature review: 2022).
https://www.uptodate.com/contents/congenital- syphilis- clinical- features- and- diagnosis.
Accessed 24 Nov 2022.
10 Congenital Syphilis andHearing Loss
https://t.me/medicina_free
3. Dobson SR, Sanchez PJ. Syphilis. In: Cherry JD, Harrison GJ, Kaplan SL, Steinbach WJ,
Hotez PJ, editors. Feigin and Cherry’s textbook of pediatric infectious diseases. 8th ed.
Philadelphia: Elsevier; 2019. p.1268–84.
4. Anteric I, Basic Z, Vilovic K, Kolic K, Andjelinovic S.Which theory for the origin of syphilis
is true? J Sex Med. 2014;11:3112–8.
5. Garrison FH.Cultural and social aspects of medieval medicine. In: An introduction to the history of medicine. 4th ed. Philadelphia: WB Saunders Co.; 1929. p.168–92. https://ia804702.
us.archive.org/29/items/in.ernet.dli.2015.63857/2015.63857.An- Introduction- To- TheHistory- Of- Medicine_text.pdf. Accessed 24 Nov 2022.
6. Pusey WA. The history and epidemiology of syphilis. Springeld: Charles C. Thomas
Publisher; 1933. p.1–132. https://iiif.wellcomecollection.org/pdf/b29931873 Accessed: Nov
24, 2022.
7. Hernandez J.Syphilis in sixteenth-century Europe. In: Bryn JP, editor. Encyclopedia of pestilence, pandemics, and plagues. Westport: Greenwood Press; 2008. p.691–4. https://www.aca-
demia.dk/MedHist/Sygdomme/PDF/Encyclopedia_of_Pestilence_Pandemics_and_Plagues.
pdf. Accessed 24 Nov 2022.
8. Abel EL.Syphilis: the history of an eponym. Names. 2018;66(2):96–102. https://ans- names.
pitt.edu/ans/article/view/2146/2145. Accessed 24 Nov 2022.
9. Castiglioni A.Contagious disease. Syphilis. Sweating sickness. Exanthematic typhus. Sanitary
legislation. In: Castiglioni A, Krumbhaar EB, editors. A history of medicine. 2nd ed. NewYork:
Alfred A.Knopf Inc.; 1947. p.453–70.
10. Rac MWF, Stafford IA, Eppes CS.Congenital syphilis: a contemporary update on an ancient
disease. Prenat Diagn. 2020;40:1703–14.
11. Rowley J, Vander Hoorn S, Korenromp E, et al. Chlamydia, gonorrhea, trichomoniasis
and syphilis: global prevalence and incidence estimates, 2016. Bull World Health Organ.
2019;97:548–62.
12. American Academy of Pediatrics. Syphilis. In: Kimberlin DW, Barnett ED, Lyneld R, Sawyer
MH, editors. Red book: 2021–2024 report of the committee on infectious diseases. 32nd ed.
Itasca: American Academy of Pediatrics; 2021. p.729–44.
13. Slutsker JS, Hennessy RR, Schillinger JA.Factors contributing to congenital syphilis cases—
New York City, 2010–2016. MMWR Morb Mortal Wkly Rep. 2018;67:1088–93.
14. Centers for Disease Control and Prevention. Preliminary 2021 sexually transmitted disease
surveillance data (last reviewed: Sep 1, 2022). https://www.cdc.gov/std/statistics/2021/default.
htm. Accessed 24 Nov 2022.
15. Kollmann TR, Dobson SRM.Syphilis. In: Wilson CB, Nizet V, Maldonado YA, Remington JS,
Klein JO, editors. Remington and Klein’s infectious diseases of the fetus and newborn infant.
8th ed. Philadelphia: Elsevier; 2016. p.512–43.
16. Cooper JM, Sánchez PJ.Congenital syphilis. Semin Perinatol. 2018;42:176–84.
17. Shefeld JS, Sanchez PJ, Morris G, et al. Congenital syphilis after maternal treatment for
syphilis during pregnancy. Am J Obstet Gynecol. 2002;186:569–73.
18. Hussain SA, Vaidya R. Congenital syphilis. In: Stat Pearls [Internet]. Treasure Island: Stat
Pearls Publishing. 2022 (updated: Oct 2, 2022). https://www.ncbi.nlm.nih.gov/books/
NBK537087. Accessed 24 Nov 2022.
19. Hussein K, Peter C, Sedlacek L, et al. Necrotizing funisitis: histopathological indicator of
occult congenital syphilis. Pathologe. 2017;38:312–6.
20. Gomez GB, Kamb ML, Newman L, etal. Untreated maternal syphilis and adverse outcomes of
pregnancy: a systematic review and meta-analysis. Bull World Health Organ. 2013;91:217–26.
21. Pillay S, Tooke LJ. Symptomatic congenital syphilis in a tertiary neonatal unit in Cape
Town, South Africa: high morbidity and mortality in a preventable disease. S Afr Med
J. 2019;109:652–8.
22. Velaphi S, Sanchez PJ. Syphilis. In: Hutto C, editor. Congenital and perinatal infections: a
concise guide to diagnosis. Totowa: Humana Press; 2006. p.199–215.
23. Dobson SR. Congenital syphilis: evaluation, management, and prevention. In: Kaplan
SL, Weisman LE, editors. UpToDate. Waltham: UpToDate (updated: Mar 26, 2021; lit-
145
146
https://t.me/medicina_free
erature review: 2022). https://www.uptodate.com/contents/congenital- syphilis- evaluation-
management- and- prevention. Accessed 24 Nov 2022.
24. Yang H, Zhang H, Wang C, etal. An analysis of the clinical features of children with early
congenital syphilis and syphilitic hepatitis. BMC Pediatr. 2021;21:498–503.
25. Saini AG, Kamila G, Vyas S. Severe microcephaly, intellectual disability and epilepsy: the
ravages of congenital syphilis. BMJ Case Rep. 2021;14:e244203.
26. Singh AE, Romanowski B. Syphilis: review with emphasis on clinical, epidemiologic, and
some biologic features. Clin Microbiol Rev. 1999;12:187–209.
27. Centers for Disease Control and Prevention. Syphilis (Treponema pallidum) 2018 case deni-
tion. https://ndc.services.cdc.gov/case- denitions/syphilis- 2018. Accessed 24 Nov 2022.
28. Martin J, Kopplin L, Costakos D.Syphilitic interstitial keratitis treated with topical tacrolimus.
Am J Ophthalmol Case Rep. 2021;23:101175.
29. Rawstron SA, Hawkes SJ. Treponema pallidum (syphilis). In: Long SS, Prober CG, Fischer
M, Kimberlin DW, editors. Principles and practice of pediatric infectious diseases. 6th ed.
Philadelphia: Elsevier; 2023. p.986–93.
30. Kaspar A, Newton O, Kei J, Driscoll C, Swanepoel DW, Goulios H.Prevalence of otitis media
and risk factors for sensorineural hearing loss among infants attending child welfare clinics in
the Solomon Islands. Int J Pediatr Otorhinolaryngol. 2018;111:21–5.
31. Besen E, Paiva KM, Hillesheim D, Cigana LB, Haas P.Congenital syphilis associated with
hearing screening failure in southern Brazilian newborns. Braz J Otorhinolaryngol. 2022;88
Suppl 3(Suppl 3):S20–4.
32. Tamari MJ, Itkin P.Penicillin and syphilis of the ear. Eye Ear Nose Throat Mon. 1951;30:252–61.
33. Karmody CS, Schuknecht HF. Deafness in congenital syphilis. Arch Otolaryngol.
1966;83:18–27.
34. Gleich LL, Urbina M, Pincus RL.Asymptomatic congenital syphilis and auditory brainstem
response. Int J Pediatr Otorhinolaryngol. 1994;30:11–3.
35. Chau J, Atashband S, Chang E, Westerberg BD, Kozak FK.A systematic review of pediatric sensorineural hearing loss in congenital syphilis. Int J Pediatr Otorhinolaryngol.
2009;73:787–92.
36. Arain Z, Abbas Y, Adams A.Pediatric otosyphilis: an unusual cause of conductive hearing
loss. Radiol Case Rep. 2019;15:65–70.
37. Ramchandani MS, Litvack JR, Marra CM.Otosyphilis: a review of the literature. Sex Transm
Dis. 2020;47:296–300.
38. Becker GD.Late syphilitic hearing loss: a diagnostic and therapeutic dilemma. Laryngoscope.
1979;89:1273–88.
39. Kivekas I, Vasama JP, Hakomaki J. Bilateral temporal bone otosyphilis. Otol Neurotol.
2014;35:e90–1.
40. Hahn RD, Rodin P, Haskins PL.Treatment of neural deafness with prednisone. J Chronic Dis.
1962;15:395–410.
41. Brouwer MC, McIntyre P, Prasad K, van de Beek D.Corticosteroids for acute bacterial meningitis. Cochrane Database Syst Rev. 2015;2015(9):CD004405.
42. Catueno S, Tsou PY, Wang YH, Becker E, Fergie J.Congenital syphilis and the prozone phenomenon: case report. Pediatr Infect Dis J. 2022;41:e268–70.
43. Zhang Y, Dai X, Ren Z, Lin H, Cao W, Ye X.A novel nested real-time polymerase chain reaction for Treponema pallidum DNA in syphilis biospecimens. Sex Transm Dis. 2019;46:41–6.
44. Tong ML, Zhang HL, Zhu XZ, etal. Reevaluating the sensitivity of the rabbit infectivity test
for Treponema pallidum in modern era. Clin Chim Acta. 2017;464:136–41.
45. Giacani L, Lukehart SA.The endemic treponematoses. Clin Microbiol Rev. 2014;27:89–115.
46. French P, Gomberg M, Janier M, etal. IUST: 2008 European guidelines on management of
syphilis. Int J STD AIDS. 2009;20:300–9.
47. Mohammad Hussein PMN, Kew ST, Nang KM, et al. Skeletal manifestations of congenital
syphilis: rare but clinically relevant. Radiol Case Rep. 2021;16:3635–7.
48. Li Y, Connelly SV. Pseudoparalysis of Parrot—re-emergence of the great mimicker. Am J
Emerg Med. 2021;48:378.
E. M. Kara et al.
10 Congenital Syphilis andHearing Loss
https://t.me/medicina_free
49. World Health Organization. WHO guidelines for the treatment of Treponema pallidum (syphilis). Geneva: WHO. 2016. p. 1–60. https://apps.who.int/iris/bitstream/han
dle/10665/249572/9789241549806- eng.pdf. Accessed 24 Nov 2022.
50. Workowski KA, Bolan GA, Centers for Disease Control and Prevention. Sexually transmitted
diseases treatment guidelines, 2015. MMWR Recomm Rep. 2015;64:1–137.
51. Walker GJ, Walker D, Franco D, Grillo-Ardila CF.Antibiotic treatment for newborns with
congenital syphilis. Cochrane Database Syst Rev. 2019;2(2):CD012071.
52. Woods CR. Syphilis in children: congenital and acquired. Semin Pediatr Infect Dis.
2005;16:245–57.
53. Centers for Disease Control and Prevention. Congenital syphilis—United States, 2003-2008.
MMWR Morb Mortal Wkly Rep. 2010;59:413–7.
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Congenital Zika Virus Infection
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andHearing Loss
MuhammetDilber, CemalCingi, andDesiderioPassali
11.1 Introduction
Zika virus (ZIKV) is a member of the family Flaviviridae. In common with the other
members of this group, it is a single-stranded RNA virus with an envelope and an
icosahedral morphology [1]. The viral envelope consists of a lipid membrane
densely studded with projecting glycoproteins [1].
In the majority of patients, ZIKV infections are of mild severity and resolve
spontaneously. The time from initial viral exposure to the rst appearance of symptoms is approximately 3–14days [2]. The features of Zika infection share similarities with other arthropod-borne viral diseases, although a maculopapular exanthem,
probably due to an immune reaction, is generally the key feature [2]. One feature
differentiating ZIKV from other arthropod-borne infections is that it may also be
transmitted by sexual contact. There is an association of congenital central nervous
system anomalies and maternal ZIKV infection in the initial trimester of pregnancy.
The earliest description of ZIKV dates from 1947, when a rhesus macaque held
in captivity in the Zika forest, Entebbe, Uganda, was found to be pyrexial and the
causative pathogen was identied as a newly discovered virus. This was followed
11
M. Dilber (*)
The Dilber Ear, Nose, and Throat Diseases and Surgery Clinic, İstanbul, Türkiye
e-mail: dilbermuhammet7@gmail.com
C. Cingi
Department of Otorhinolaryngology, Faculty of Medicine, Eskişehir Osmangazi University,
Eskişehir, Türkiye
e-mail: cemal@ogu.edu.tr; ccingi@gmail.com
D. Passali
International Federation Oto-Rhino-Laryngological (ORL) Societies (IFOS), Rome, Italy
e-mail: d.passali@virgilio.it
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
A. E. Arısoy et al. (eds.), Hearing Loss in Congenital, Neonatal and Childhood
Infections, Comprehensive ENT, https://doi.org/10.1007/978-3-031-38495-0_11
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the next year by the discovery that the Aedes africanus mosquito was the vector
within the Zika forest. The existence of Zika infection in humans was conrmed in
1952 [1, 3]. Since then, Zika infection has been noted in several areas beyond
Africa, notably Micronesia and French Polynesia [4, 5]. A major epidemic occurred
between 2015 and 2016, in the Americas, with the majority of cases in the United
States found to be linked to travel. The World Health Organization (WHO) declared
a public health emergency in 2016in response to this epidemic [6]. Conrmed Zika
infections fell after 2017, and in 2021, it was reported that there were no current
new infections occurring anywhere in the world [7, 8].
M. Dilber et al.
11.2 Pathophysiological Features
The ZIKV genome consists of 10,700 base pairs, with structural and nonstructural
regions. The structural regions code for three structural proteins, C, prM and E,
standing for core, pre-membrane, and envelope. The nonstructural region encodes
seven proteins of nonstructural kind. The virus gains entry to the cell by attaching
itself to a transmembrane tyrosine kinase enzyme, the AXL receptor. This involves
the prM and E proteins. The virus is absorbed by endocytosis, after which the
nucleocapsid coat is removed to allow viral RNA to enter the cytoplasmic compartment. This RNA is a negative sense strand, from which positive sense RNA is transcribed by a complex of proteins of viral origin encoded by the nonstructural region
of the viral genome. The viral proteins are synthesized as a polyprotein, which then
undergoes modication within the endoplasmic reticulum, forming virions. These
are then released from the infected cell within secretory vesicles. The nonstructural
viral proteins and the structural core protein cause the cell to stop progress through
the cell cycle and eventually to undergo programmed cell death (i.e., apoptosis) [1, 2].
Cryogenic electron microscopic techniques were used by Sirohi etal. to determine the structure of the fully formed Zika virus. The overall structure is similar to
that of the other aviviruses but displays a unique structure in the Asn154 glycosylation site on the glycoproteins, which make up the viral envelope. This site consists
of ten amino acids. ZIKV has an icosahedral shell, consisting of 180 envelope proteins. The glycosylation site appears to be how the virus binds to human cells before
entry [9].
Phylogenetic analysis reveals that the ZIKV has two separate lineages, one in
Asia and one in Africa, and has three different genotypes, namely, West, East
African, and Asian. The Asian variant originated in Asia but was then transmitted to
the Americas and islands of the Pacic. So far, the extent to which the viral lineage
affects the clinical picture is unclear. One hypothesis links the Asian variant to
severe outbreaks and may result in congenital defects, rather than death of the fetus,
whereas the African variant may cause an acute infective episode that harms the
outcome of pregnancies [10].
ZIKV has evolved to be able to replicate effectively in a variety of animal hosts,
both arthropods and vertebrates. It has a tropism in humans for certain tissues such
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as the skin, blood, placenta, testis, and retina. It also infects neural stem cells and
neuroprogenitor cells. The virus can also replicate inside monocytes, which means
it can be transported through the placental and blood–brain barriers. Cells respond
to ZIKV infection by dying, either through apoptosis or necrosis. Both congenital
neurological anomalies and intrauterine death can be explained in this way, the former resulting from death of neuroprogenitor cells and the latter through placental
damage [11].
The initial response to ZIKV infection occurs through activation of innate
immunity. Viral replication is inhibited through secretion of type 1 interferons,
which induce expression of specic genes. The viral nonstructural proteins can
block the signals leading to interferon expression and synthesis of interferon gene
products, thereby evading attack by the immune system. It has been shown that
ZIKV can prevent stress granules being formed and take control of nonsensemediated mRNA decay, thereby increasing the ability of the virus to make copies
of itself. The exact mechanisms by which ZIKV avoids destruction by the immune
system are, however, still imperfectly understood, and more research is needed in
this area [8, 12].
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11.3 Epidemiological Features
There are few data available on how prevalent ZIKV infections are worldwide. The
picture is complicated by asymptomatic infections, clinical confusion with other
diseases caused by aviviruses (such as dengue and chikungunya), and problems
with achieving diagnostic certainty [8].
A study that collated evidence from reports of epidemics, entomological research
and serological prevalence data in July 2019 ascertained that ZIKV had been found
in 87 different countries or territories, covering Africa, North and South America,
Southeast Asia, and the Western Pacic, and in humans, monkeys, and mosquitoes [3].
Ugandan data from 1952 indicated a prevalence of 6.1% for Zika infection,
based on a sample of 99 individuals [13]. When patients in Java, Indonesia, admitted to hospital for pyrexia were examined between 1977 and 1978, ZIKV was identied in 7.1% of cases [14]. A West African study from 2007 to 2012 covering Mali,
Gambia, and Senegal found serological evidence of ZIKV infection in 20–22% of
those tested [2].
There has been an extension in the range of ZIKV infection since 1947, when the
virus was rst identied in Africa. Its range now included Southeast Asia and North
and South America. There were occasional reports of ZIKV infection prior to 2007.
In that year, an epidemic of ZIKV infection affected some 73% of the inhabitants of
the island of Yap in Micronesia. The virus was transmitted by the Aedes hensilli
mosquito [5]. There were Zika outbreaks in French Polynesia, New Caledonia, the
Cook Islands, Easter Islands, and other islands of the Pacic between 2013 and
2015 [6]. Guillain-Barré syndrome was noted to occur as a complication of Zika
infection in cases from French Polynesia [8].
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M. Dilber et al.
11.4 Prognosis
The majority of ZIKV infections are of mild severity and resolve without intervention. The lack of severe symptoms probably explains why at least 80% of infections
do not come to clinical attention [2].
Rarely, ZIKV infections cause severe nervous system complications, such as
Guillain-Barré syndrome [2, 15].
The most concerning aspect of ZIKV infections may, however, be when they
occur in pregnant women. In these cases, the risk of an adverse outcome rises, and
transmission from mother to fetus carries a poor prognosis in the long term [14, 16].
Furthermore, infection with ZIKV causes temporary infertility [8].
11.5 Transmission
Transmission of ZIKV can occur both via vectors and in other ways [8].
11.5.1 Transmission Via Vectors
In common with several other aviviruses, transmission may occur via an arthropod
vector [17], especially different species within the mosquito genus Aedes, such as
A. aegypti, A. africanus, A. luteocephalus, A. albopictus, A. vittatus, A. furcifer,
A. hensilii, and A. apicoargenteus [1, 2, 5, 18]. Isolation of ZIKV is also reported
from the southern house mosquito, Culex quinquefasciatus. The virus passes from
human or other vertebrate hosts into mosquitoes and is then passed onto another
host. ZIKV transmission occurs enzootically among nonhuman primates, while
human-to-human transmission is described as the urban life cycle. Two species,
A. aegypti and A. albopictus, are generally resident in tropical and subtropical areas,
although they may also exist elsewhere. The former species is a major disease vector, whereas the latter has only occasionally been implicated as vector. The geographical areas of the United Staes where ZIKV has the potential to become endemic
have been mapped by the Centres for Disease Control, based on the likely habitats
for A. aegypti or A. albopictus.
For the United States, new cases are most common between June and October,
corresponding to the period when mosquitoes are most likely to feed on human
blood. ZIKV resides in the salivary glands of the arthropod vector, passing via the
bite into the host’s circulation, whence it can arrive at the skin and other tissues for
which it has a tropism [19].
11.5.2 Viral Transmission Not Involving Vectors
Analysis of ZIKV epidemics has revealed that the virus may also be transmitted
without the need for a vector [8].
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For pregnant women infected at any stage of the pregnancy, the risk of transmission to the fetus is between 20 and 30%. The initial trimester is the period during
which vertical transmission produces the gravest consequences and is when Zika
syndrome occurs. Despite the isolation of ZIKV from breast milk, there are no data
to show that the virus may be transmitted to infants through nursing. Accordingly,
even where a mother is denitely or potentially infected by ZIKV, breastfeeding
should continue, since its benets exceed the risks [2, 20].
Within the rst month of becoming infected, ZIKV is found in the semen of
50–60% of infected male patients, with a case recorded where the virus could still
be isolated after 281days. There are reports indicating transmission of ZIKV from
a male to female sexual partner in the United States and French Polynesia.
Furthermore, cases where the virus has been transmitted sexually from a woman to
a man, or between men, have also been described. It has been calculated that the
period between 32 and 44 days after initial symptoms appear in ZIKV-infected
patients is the most likely time for sexual transmission to occur [1, 2, 21].
There is a brief window of opportunity for serological detection of ZIKV in
acutely ill patients. RNA from ZIKV has been estimated to be present in approximately 1in 100 donated blood samples, which means that iatrogenic transmission
via transfusion is still a potential problem. Although ZIKV has also been detected in
other body uids (urine, saliva) or solid organs, it does not appear currently that the
virus is transmitted during organ transplantation [1, 2, 8, 22].
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11.6 Symptomatology andPhysical Findings
Cases of VIKV are usually symptomatic for between 2days and 1week [2]. The
most common presentation is an exanthem. Other frequent ndings are pyrexia,
joint pain (affecting the nger and toe joints), headache localized to behind the eyes,
and conjunctival inammation [1, 5, 15].
On rare occasions, ZIKV infection triggers Guillain-Barré syndrome [2, 15].
There is a case report in the literature of a young doctor with no other health problems who suffered hypertensive iridocyclitis, probably caused by infection with
ZIKV [13].
The most usual clinical picture is one of swift, total resolution of symptoms. A
study in 2007 where ZIKV infection cases from Yap Island, Micronesia, were retrospectively reviewed, found no patient had been admitted to hospital and no hemorrhage or fatality had occurred [5, 8].
11.7 Factors toConsider inClinical Approach
It is challenging to conrm a diagnosis of ZIKV infection by laboratory testing,
since the tests used have low sensitivity and specicity and the frequency of infections is generally low. There are both molecular and serological techniques available for diagnostic conrmatory purposes [23]. The standard way to conrm the
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