and Antimicrobials for viruses)
Table of contents :
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Generalities for viroses
Web resources |
,
acute
bronchitis
or interstitial
pneumonia
,
acute
bronchitis
or interstitial
pneumonia
("recruit fever")
or interstitial
pneumonia
("recruit fever"),
acute
bronchitis
or interstitial
pneumonia
("recruit fever")
in babies
with dissemination or urinary
tract infections (UTI)
in immunocompromised hosts
with dissemination or urinary
tract infections (UTI)
in immunocompromised hosts
formation hence affecting presentation of the immunoproteasome-dependent
epitope E1B. E1A interacts with the 19S S4
ATPase subunit of the 26S
proteasome.
with dissemination or urinary
tract infections (UTI)
in immunocompromised hosts
or Bordetella parapertussis,
although evidence of other infectious agents, such as adenoviruses types
1, 2, 3, 5, and 6, can be demonstrated
(RR = 5-6)
with dissemination or urinary
tract infections (UTI)
in immunocompromised hosts
,
acute
bronchitis
or interstitial
pneumonia
("recruit fever")
after 24-72 hours incubation => cholangiohepatitis
occurs in immunocompromised hosts as a result of ascending infection from
the gastrointestinal tract to the biliary tree.
as receptor).).
Respiratory infections in children are short-lived and rarely life-threatening.
Outbreaks of adenovirus respiratory infections have been common among military
recruits (mainly types 4, 7, 14 and 21), where rates of hospitalisation
have reached 20%. As a result vaccines were developed against adenovirus
types 3, 4, 7 and 21, but later withdrawn. Most outbreaks of pharyngoconjunctivital
fever in school-age children have occurred occur during the summer, whereas
the outbreaks among military recruits have occurred during winter, probably
reflecting a different mode of transmission. Adenovirus types 8, 9 and
11 have been associated with outbreaks of keratoconjunctivitis (also known
as shipyard eye) in adults. However, whereas multiple serotypes from different
species have been described as causing cases or limited, irregular outbreaks
of ocular disease in humans, there are only a few serotypes that regularly
cause larger outbreaks or epidemics. The 2 types of ocular disease that
are commonly caused by adenoviruses are pharyngoconjunctival
fever (PCF)
and epidemic
keratoconjunctivitis (EKC).
An interesting observation is that the 3 serotypes that cause EKC (Ad8,
Ad19, and Ad37) use a cellular receptor (sialic acid) that is different
from the cellular receptors used by other adenoviruses (CAR or CD46)
.)
out of 27 in a wildlife shelter in Nantou County were put down after they
were diagnosed as carriers
,
and death
: the BTLA binding site on HVEM overlaps with the binding site for the
gD, but is distinct from where LIGHT binds, yet glycoprotein D inhibits
the binding of both ligands, potentially nullifying the pathwayref.
Coreceptors : herpesvirus
entry protein B (HveB) / poliovirus receptor-related 2 (PVRL2) / CD112
/ CD155 and herpesvirus
entry protein C (HveC) / poliovirus receptor-related 1 (PVRL1) / nectin-1
/ herpesvirus Ig-like receptor (HIgR) (that confined with E-cadherin
to adherens junctions in epithelial cells is not very accessible to virus,
whereas dissociation of cell junctions releases nectin-1 to serve more
efficiently as an entry receptor)
of viral infection.
and oropharyngitis
in babies before age 3 (the most common kind of primary infection) => eschar
(=> squamous lip carcinoma),
self-limiting within 10-14 days.
and sometimes chills occur.
that erode and spread. The lower lip is more commonly affected than the
upper lip.)
in individuals who have active or quiescent atopic
dermatitis (AD).
on the finger or hand due to bacterial superinfection, often seen in health
cares workers (dentists, ..) who have a tendency to touch HSV lesions without
dressing gloves)
in adults => epilepsy
(?)
(type II hypersensitivity mediated by Th1
effector cells) leading to scarring, opacity, and blindness, and it is
an important problem in common corneal surgeries or acute monolateral
follicular conjunctivitis.
In the preclinical phase, when HSV-1 replicates in the corneal epithelium,
neutrophils invade the underlying corneal stroma. This transient response,
triggered by replicating virus, is thought to control HSV replication and
limit viral spread into peripheral tissues. During the clinical phase,
a second wave of inflammatory cells, predominantly consisting of neutrophils,
infiltrates the corneal stroma and destroy it. Paradoxically, virus antigens
are largely focused in the epithelial layer of the cornea and not in the
stromal layer, and viral antigens are eliminated before stromal inflammation
develops. It is not clear what drives inflammation, whether viral antigens
are necessary, or how viral antigens reach the stroma. It has been proposed
that HSV travels from the corneal epithelium to sensory ganglia then returns
to the stroma to cause disease. However, there is also evidence of HSV
DNA and infectious virus persistent in corneas, and HSV can be transmitted
to transplant recipients. US9- HSV mutant, that had diminished
capacity to move in neuronal axons, replicated and spread normally in the
mouse corneal epithelium and to the trigeminal ganglia. However, US9-
HSV
was unable to return from ganglia to the cornea and failed to cause periocular
skin disease, which requires zosteriform spread from neurons. Nevertheless,
US9- HSV caused keratitis. Therefore, herpes keratitis can occur without
anterograde transport from ganglia to the cornea, probably mediated by
virus persistent in the cornearef.,
interstitial
pneumonia
: lethality 50%)
=> vesicles
(?)
(?)
(Lipschutz inclusions), owl-eye
inclusions
is more susceptible to HSV-1 encephalitis than Aotus
trivirgatus
(expensive, difficult to obtain and to maintain in captivity)
.
;
alcoholic povidone-iodineref.
Coreceptors : herpesvirus
entry protein B (HveB) / poliovirus receptor-related 2 (PVRL2) / CD112
/ CD155 and herpesvirus
entry protein C (HveC) / poliovirus receptor-related 1 (PVRL1) / nectin-1
/ herpesvirus Ig-like receptor (HIgR)
,
vulvovaginitis,
balanoposthitis,
non-gonococcal
urethritis (NGUs),
proctitis
(severe in male homosexuals). The lesions are very superficial (unlike
chancroid or syphilis, whose lesions are lumpy). The primary lesions stay
for 2-3 weeks, but recurrent usually heal within 3-5 days.,
and visceral disease (interstitial
pneumonia,
hepatic necrosis). If the mother has been seropositive for some time before
the birth, then transplacental IgG serve as a protective mechanism for
the newborn. >50% mortality.,
seborrhoic
dermatitis,
pemphigus
or Wiskott-Aldrich
syndrome
=> generalized herpes (including erythema
multiforme,
herpetic
stromal keratitis (HSK),
retinal necrosis)
when the virus travels up the nerve to the brain instead of down towards
the lip (lethality 50%)
: recurrent aseptic meningitis characterized by headache,
malaise, meningeal sings, and monocytes in the CSF.
and acute pharyngitis
in adults following oro-genital contacts => eschar
(=> squamous lip carcinoma)
(priming effect for HPV-6, HPV-10,
HPV-11,
HPV-16,
and HPV-18 ?),Cowdry
type A inclusion bodies
(Lipschutz inclusions).
.
)
or cidofovir
(if resistance occurs => foscarnet),
idoxuridine,
vidarabine
and trifluridine.
=> vesicles
(Sklowsky's symptom : when light pressure with the index finger
is made upon the healthy skin near, and then over, a vesicle in varicella,
the wall of the vesicle easily collapses and the contents are discharged)
=> pustules
with "starry sky" look (contemporaneous presence of papulae, vesicles
and scubs on whole body). + salicylates (+ Influenzavirus
A H3N2 ?) => Reye's
syndrome
. Sequelae : vesicles,
impetigo,
neuraxitis,
acute
glomerulonephritis,
acute
hepatitis,
keratitis,
interstitial
pneumonia
(1%, expecially in immunocompromised adults => death due to respiratory
failure), postvaricella
purpura fulminans
(due to autoimmune thrombocytopenia
and DIC),
lupus anticoagulant (LAC), cerebellitis
(=> ataxia), post-infective encephalitis
(PIE : 1 case out of 4,000-10,000), overinfection by Streptococcus
pyogenes
(expecially necrotizing fasciitis and TSLS) => thrombosis. Lifelong presence
of neutralizing antibodies prevents reinfection. Virus undergoes latency
in satellite cells of a sensitive ganglion.
month 4 => eye, brain and limbs injuries in newborn
and iridocyclitis)
if reactivation occurs in geniculate ganglion of facial nerve
if reactivation occurs in uditive nerve
recipients, visceral disease may precede or occur in the absence of the
characteristic signs on the skinref1,
ref2,
ref3,
ref4.
In such cases, in which patients present with severe unexplained abdominal
pain, diagnosis and treatment are usually delayed until signs of the infection
appear on the skin or, in the absence of a rash, the diagnosis is made
at necropsy. In allogeneic BMT recipients, the symptoms may be misdiagnosed
as graft-versus-host disease, and immunosuppressive treatment instituted,
with potentially grave consequencesref.
In view of the significant morbidity and mortality, early diagnosis of
visceral involvement of herpes zoster is highly desirable. A case series
of 4 patients with visceral herpes zoster was reported in whom large concentrations
of DNA from VZV were detectable in blood by PCRref
before signs of infection appeared on the skin, thus enabling early diagnosis
and treatmentref,
encephalitis,
Cowdry
type A inclusion bodies
protects from primary infection but not from reactivations; the only way
to prevent shingles is eradication via massive antiviral drugs (vidarabine,
acyclovir)
while having chickenpox, before the virus shelters into ganglia (where
drugs can't reach it).
(prodrug : valacyclovir) or famciclovir
in a carrier state for long periods of time and then be reactivated. Once
introduced into a herd the virus usually remains there and it can continually
affect reproductive performance at varying levels. The virus can survive
for up to 3 weeks outside the pig. The virus crosses the uterus and placenta
and infects the foetuses.
,
nervous signs, reproductive failure, abortions, mummified piglets, stillbirths,
birth weak litters.,
Felis
catus,
... : nervous signs, death.,
sneezing, coughing, interstitial
pneumonia.
Nervous signs including incoordination, fits, Aujeszky's itch / mad
itch, and meningitis.
Some strains of the virus can cause severe respiratory disease and others
severe acute
rhinitis.
Usually low mortality. However, the pathogenicity to human is controversial
: maybe it is dangerous only for immunocompromised hosts.
on monocytes (and DCs) and neutrophils (leukotropism)
and inhibits NK cell cytotoxicityref
and MICB,
retaining them in the cell and effectively masking NK-cell recognition.
gp40,
the ortholog murine cytomegalovirus (MCMV) protein, disrupts the RAE-1-NKG2D
interaction in mice by sequestering RAE-1 molecules, but not H60.
ortholog. that induces retention of MHC class II+ vesicles in
an abnormal perinuclear distribution in DCs.,
modulating the host antiviral response even before the newly infecting
viral genome becomes transcriptionally activeref.
products, resulting in the rapid degradation of HLA-DRa
and HLA-DMa in DCs.
complexes in the ER.
products to Derlin-1, a human homologue of yeast Der1p, a protein essential
for the degradation of a subset of misfolded ER proteins catalysed by US11,
but not by US2ref.
Derlin-1 interacts with US11, a virally encoded ER protein that specifically
targets MHC class I heavy chains for export from the ER, as well as with
VIMP, a novel membrane protein that recruits the cytosolic p97 ATPase and
its cofactorref.
US11 transports MHC class I H chains back into the
cytosol, where they are deglycosylated by host N-glycanase and then
degraded by the 26S
proteasome|
|
|
|
|
| 18÷29 |
47.4 %
|
93.3 %
|
35.7 %
|
| > 30 |
62.5 %
|
93.8 %
|
45.3 %
|
| every age |
54.3 %
|
93.5 %
|
42.7 %
|
(?)
with no
pharyngotonsillitis
and Downey type I atypical lymphocytes => immunodeficiency,
cold
agglutinin disease.
Samples for direct diagnosis vary with time : oropharyngeal swab => blood
=> urine. Virus undergoes latency in PBMCs.
(24% higher likelihood than unaffected ones)
or syndrome : cytomegalovirus mononucleosis occurring about 3 to 6
weeks after extracorporeal circulation or multiple blood transfusions in
open heart or other surgical procedures
(Guillain-Barré
syndrome)
and cytomegalovirus chorioretinitis
("pizza pie" look) fist monolateral, then bilateral
:
: CMV seromismatched patients (donor+/recipient-
or D+/R-) have a 60-80% probability of primary CMV
disease and a significantly higher rate of acute rejection than non-seromismatched
patients (72% vs. 54.2%, P=0.005). Using multiple logistic regression,
CMV seromismatch, delayed graft function, and biological induction were
identified as independent predictors of acute rejection. The adjusted odds
ratios for these are 2.28, 1.65, and 0.52, respectively. In such cases
chemoprophylaxis is justified, at least in those patients who are are found
to have 1 or more pp65+ cells per 150,000 peripheral WBCs examined
(preemptive therapy)
: the greater the viral load, the higher the risk of vascular lesion
rejection
chronic rejection
chronic rejection,
owl-eye
inclusions
is not effective due to lack of tk. Effectiveness of ganciclovir
oral chemotherapy (5 mg / kg IV or 1000 mg q8h PO) has been shown in
SYNTEX 1654 trial (patients affected by both HIV-1
and CMV) : if resistance occurs => foscarnet..
Treatment of pregnant women with primary CMV infection with CMV-specific
monthly hyperimmune globulin (100 U/kg i.v.). is safe, and the findings
of this nonrandomized study suggest that it may be effective in the treatment
and prevention of congenital CMV infection. A controlled trial of this
agent may now be appropriateref1,
ref2
(expressed ubiquitously in human tissues); it induces syncytium formation
of diverse human cells 2 h after infection by fusion from without (FFWO)
ref
(at a lesser extent than HHV-7ref),
but so far there is not enough evidence for a pathogenetic association
of HHV-7 with this exanthematic skin diseaseref
and 39% of those of Hodgkin's lymphoma;
however, no correlation of activation status with pathological types of
Hodgkin's disease and between copy numbers in peripheral blood mononuclear
cell DNA and the corresponding plasma DNA was noticeableref.
(?)
mediated CPE in super-infections of CD4+ T-lymphocytes : a 3.9-kbp
SalI-L DNA fragment spanning the junction of the direct repeat left (DRL)
and unique long segment (UL) regions of HHV-6 up-regulates HIV-1 LTR CAT
10-15 fold in both monkey CV-1 and human T Jurkat cellsref.
(expressed ubiquitously in human tissues); it induces syncytium formation
of diverse human cells 2 h after infection by fusion from without (FFWO)
-like
syndrome of infants and young children (expecially between month 6 and
age 2) after 5-15 days incubation; after a high fever
of 3 to 4 days' duration, occipital
lymphadenitis,
laterocervical
lymphadenitis
and retroauricular
lymphadenitis
the temperature suddenly drops to normal; either shortly before, simultaneously
with, or shortly after this happens, a macular or maculopapular rash appears
on the trunk and spreads to other areas for 1-2 days. Downey type
III atypical lymphocytes. Complications
:
(=> febrile convulsions (with and without exanthem)); usually fatal when
it is resistant to antiviral drugs unless treated with donor
lymphocyte infusions (DLIs)ref
or chronic iridocyclitis may occur
antigen (may contribute to the pathogenesis of nasopharyngeal carcinoma
in cooperation with EBVref)
and activates lytic cycle replication of HHV-8
/ KSHVref
(?)
and papular-purpuric
gloves-and-socks syndrome,
but has also been found to occur in normal dermal tissues. There are controversial
data on the detection of HHV-7 (at a greater extent than
HHV-6ref)
in pityriasis rosearef
(primary infection > reactivationref),
but so far there is not enough evidenceref1,
ref2,
ref3,
ref4
,
there are no data supporting a direct causative role in this lymphoma type
nor in other nodal or primary cutaneous lymphomas
,
infection of monocytic cells with HHV-7 was demonstrated, which may indirectly
influence tumor biology
.
Symptoms include paresthesia in both lower limbs, gait disturbances, visual
disturbances, abnormalities of deep tendon reflexes, and psychic disorders.
The hydroxyquinolones (especially clioquinol), taken for gastrointestinal
disorders, have been implicated as an etiologic factor
with macules
with macules
with macules
with macules
with macules
with macules
with macules
(cervical intraepithelial neoplasia (CIN))
and metastatic lymph nodes using PCRref;
in both breast and cervical cancer tissues in Norwegian women with concurrent
breast
carcinoma
and cervical
carcinomaref
with macules
(cervical intraepithelial neoplasia (CIN)). In most cases the immune
system knocks the virus out before it can do any damage. In some cases,
however, the infection becomes chronic, with measurable levels of the virus
remaining in the system. Perhaps 5% of these women will eventually develop
precancerous lesions that could lead to cervical cancer. Or at least that's
what would happen if they did not undergo routine Pap smears, which can
detect abnormal cervical tissue before it turns malignant.
with macules
with macules
with macules
with macules
with macules
with macules
with macules
of 41% of Chinese and 11% of Japanese womenref
with macules
with macules
with macules
with macules
individuals
with macules
: at present the only commercial test available is the Hybrid CaptureTM
test which will differentiate between oncogenic and non-oncogenic HPV infections.
,
for
genital warts
and ureteral stenosis
in renal transplant
recipients
in bone marrow
transplantation
recipients
ref)
in blood or biopsy, BKV nuclear inclusions can be seen
on inoculation into newborn mice
-like
decoy receptor
fill the cytoplasm and push the nucleus to the edge of the infected cells.
: clinical manifestations vary from a singular pox lesion to a generalized
form, with pox literally covering the entire animal and even found on internal
organs (e.g. lungs)
,
from which it can occasionally spread to Felis
catus,
Canis
familiaris,
Bos
taurus,
and zoo animals, including large cats and elephants.
at the site of their introduction into the skin (usually the hands: on
the thumbs, the first interdigital cleft, and the forefinger), rarely fever
and myalgia => secondary lesions occur only in individuals with immunological
deficiencies.
: a lethal disease of mice characterized by gangrene and often loss of
one or more of the feet and sometimes of other external parts, and by necrotic
areas in the liver, spleen, and other organs. Introduction of the Th2cytokineIL-4
gene in ectromelia virus further increases lethality, even in recently
immunized genetically resistant mice. These data therefore suggest that
virus-encoded IL-4 not only suppresses primary antiviral CMI but also can
inhibit the expression of immune memory responses.
: rope squirrels (Funisciurus
spp.), sun or tree squirrels, (Heliosciurus
spp.), Gambian giant rats, brushtail porcupines (Atherurus
spp.), dormice (Graphiurus
spp.), and striped mice (Hybomys
spp.)) imported from Ghana in the early April shipment, 10 died en
route to the Texas distributor or shortly after arrival, one died later
at the distributor's premises, 5 were shipped to a pet store within Texas,
9 remain alive at the distributor's premises, and from 18 to 25 of the
rats were sent to Evelee Prokes, owner of the Menagerie Hill Farm in Cincinnati,
Iowa, with 18 of those sent from Iowa to the Illinois dealer. The shipment
contained approximately 800 small mammals of 9 different species that might
have been the actual source of introduction of monkeypox. Of the 5 sold
to the pet store in Texas, one was sold to an individual. Authorities said
the animal and the owner are fine. The other 4 died. Officials said it
is not unusual for deaths to occur in wild animals brought into captivity
and that the deaths cannot be assumed to have been caused by monkeypox.
TDH officials are hopeful that testing of the live Gambian rats remaining
at the distributor's premises and of a dead Gambian rat from the pet store
that had been kept frozen may offer additional clues in the ongoing multi-state
investigation. Texas officials also said that while the prairie dogs sold
by the dealer in Illinois are believed to have come from a Texas distributor,
it is not the same dealer who supplied the Gambian rats. They said it does
not appear that the prairie dogs and Gambian rats were ever in the same
facility in Texas. All patients have had contact with animals; however,
at least 2 patients also reported contact with another patient's lesions
or ocular drainage. A total of 51 patients reported direct or close contact
with prairie dogs, and 1 patient reported contact with a Gambian giant
rat. One patient had contact with a Oryctolagus
cuniculus
that became ill after exposure to an ill prairie dog at a veterinary clinic.
No patients have died and 26% patients have been hospitalized, including
a child aged <10 years with encephalitis
(requiring hospitalization for 14 days) and second child exposed to 3 ill
prairie dogs, hospitalized with profound painful cervical and tonsillar
adenopathy and diffuse pox lesions, including lesions in the oropharynx.
Although the child had difficulty breathing and swallowing, mechanical
ventilation was not required. The date of onset for the last case was 20
Jun 2003. Studies indicate that West African and Congo basin isolates of
monkeypox virus (MPXV) are genetically distinct. Congo basin MPXV-ZAI-V79
is more virulent for cynomolgus monkeys as compared to presumed West African
MPXV-COP-58. This finding may explain the lack of case-fatalities in the
U.S. 2003 monkeypox outbreak, which was caused by a West African virus.
Virulence differences between West African and Congo basin MPXV are further
supported by epidemiological analyses that observed a similar prevalence
of antibodies in non-vaccinated humans in both regions, while > 90% of
reported cases occurred in the Congo basin, and no fatal cases were observed
outside of this region. To determine the basis for this difference in virulence,
the genomes of one human West African isolate, and 2 presumed West African
isolates were sequenced and compared the sequences to Congo basin MPXV-ZAI-96-I-16.
The analysis identified D10L, D14L, B10R, B14R, and B19R as possible virulence
genes, with D14L (ortholog of vaccinia complement protein) as a leading
candidateref.
Unpublished experiments Army researchers had done in the 1990s on such
viruses in monkeys as part of an effort to find ways to test new smallpox
vaccines showed monkeys infected with the West African strain got only
mildly ill and none died. 5 out of 6 of those given the other strain got
severely ill and all 3 that got the higher dose of it died.
(African tree squirrels (Heliosciurus and rope squirrel (Funisciurus
anerythrus)), degu (Octodon
degus), Oryctolagus
cuniculus)
via small lesions on the skin or oral mucous membranes. Person-to-person
transmission by respiratory route accounts for < 33% of observed cases
: this makes identification and containment much more accessible and the
secondary attack rate is low. Nonetheless, the fear has been expressed
that monkeypox might evolve to become an endemic human infection
(47%),
including fever
preceding or accompanying the onset of a generalized papular rash on the
head, trunk, and extremities (73%; typically progressing through stages
of vesiculation, pustule,
umbilication, and encrustation. Early lesions become ulcers
in some patients : many patients had initial and satellite lesions on palms,
soles, and extremities. Rashes are generalized in some patients); respiratory
symptoms (64%), lymphadenitis
, and sore throat (33%). The virus first localizes in mononuclear phagocytic
cells, is released into the bloodstream, and then localizes again in skin
cells. It also has a healing period that progresses more rapidly than smallpox,
but anyway still significant morbidity and mortality (1-10%, with the highest
rates among young children).
has 85% prevention rate
.
that gradually turned into raised, dark nodules
(as similar to those that develop during cowpox infection) on a finger
on each hand after working in lab with very high concentrations of recombinant
WR containing an inactivated form of the human gene for cytohesin-1,
which could impair the local immune response in the skin by interfering
with leukocyte adhesionref
which promotes corticosterone synthesis leading to immunosuppression
and IL-1R
signal transduction.-mediated
degradation of both C3b and C4b..
: a zooanthroponosis (reservoir : Bos
taurus)
,
Capra
hircus,
Ovibos
moschatus moschatus,
Rangifer
tarandus,
Rupicapra
rupicapra)
; indirect infections through contaminated knives or meat have been reported.
Transmission of orf virus to humans occurs after contact with infected
or recently vaccinated animals and/or fomites in conjunction with skin
trauma. Orf virus vaccine strains have been known to cause outbreaks among
sheepref,
and 3 of the illnesses described in this report occurred soon after vaccination
of the flock. Veterinary vaccines for orf virus use non-attenuated, live
virus preparations and are intended to produce controlled infections in
flocks (De la Concha-Bermejillo A, Ermel RW, Zhang MZ, Guo J. Contagious
ecthyma (orf) virulence factors and vaccine failure. In: Proceedings of
the United States Animal Health Association; Richmond, VA: United States
Animal Health Association; 1999). Recently vaccinated animals pose an occupational
risk to humansref.
Orf virus infection is facilitated by skin traumaref,
and previous case series have associated skin trauma with orf virus infectionref.
Trivial injury (e.g., pricks from thistle) or substantial trauma (e.g.,
bites) can facilitate transmission of orf virus. Therefore, barrier protection
(e.g., nonporous gloves) and hand washing during the care of sheep and
goats is recommended whenever feasible. These measures are especially important
for any person with a compromised immune system or a chronic skin disorder
(e.g., eczema) who has contact with overtly infected animals. Immunocompromised
persons should discuss the risks of handling orf-infected animals and infection-prevention
strategies with their primary-care physicians. Human orf virus infection
is a common yet preventable consequence of contact with sheep and goats.
Persons who are most likely to be exposed to orf virus (e.g., farm workers)
might be familiar with the infection and thus might not seek medical attention.
As a result, clinicians might not be familiar with orf virus infections,
leading to a delay in diagnosis and unnecessary antibiotic use. Public
health personnel should be cognizant that orf virus infection is similar
in appearance and risk factors to life-threatening infections such as cutaneous
anthrax and that skin trauma is a predisposing factor to infection.
.
ref
and surgical debridementref.
: a zooanthroponosis (reservoir : Bos
taurus
during milking
during 3-4 days incubation => severe headache
and backaches, itching erythema with central thickening of the prickle
cell layer => papule
which gradually enlarges to reach a maximum Ø of ~ 15 mm by the
end of the second week of infection (regional lymphadenitis
from about the 5th day following the appearance of the skin
lesion) => ulcers
during the third week => gradually heals within 5 to 6 weeks, leaving a
scar. In Kenya, the lesions were almost always solitary and were found
on the upper arm, face, neck, and truck ; conversely, in Zaire, 22% of
patients had multiple lesions (usually 2 or 3, maximum 10), mostly found
on the lower limbs, with a couple of patients reporting lesions on the
upper limbs, trunk, and head. The virus is much slower in replication than
vaccinia virus, with most of the mature progeny is retained inside the
cell..
TTV may play a role in the pathogenesis of non-A, non-B or non-C fulminant
hepatic failure. Patients co-infected with hepatitis
C virus (HCV)
and TTV have a significantly higher histological grade score than patients
with isolated HCV infection
ref
(poorly expressed on the apical surface of polarized ciliated respiratory
epithelial cells), and the FGFR-1
(ubiquitous) and avb5
integrin as coreceptorref
(lung, central nervous system, muscle and eye)ref
or g-irradiationref.
on face => arms and hips => trunk; followed by ...
of hands, knees, whistles and ankles (5-10% of babies and 50-60% of adults,
sometimes without fever
or exanthema) self-limiting with 2-21 days. Acute B19 infection can simulate
early RA
or SLE
(butterfly rash over the cheeks, cytopenia, etc.)ref1,
ref2.
In addition, there have been a few reports of erosive RA or SLE developing
shortly after a B19 infection, with positive PCR tests for B19 DNA in synovial
tissue or blood cells. Studies in large series indicate that B19 is probably
an extremely rare cause of RA or SLE. Vasculitides affecting the small
vessels (Henoch-Schonlein
purpura,
Wegener's
granulomatosis),
medium-sized vessels (periarteritis
nodosa),
and large vessels (giant
cell arteritis)
can occur after B19 infection
for 7-10 days (it undergoes chronicization in immunocompromised individual);
persistent infection in immunocompromised patients can lead to chronic
bone marrow failure
=> fetal hydrops,
fetal death, and spontaneous abortion and acute
hepatitis
(liver is the fetal hematopoietic organ).methods
must be applied.Epidemiology : regions of the Rocky Mountains area and Pacific slope of the USA and Canada, where it causes CTF, a human disease initially confused with a mild form of Rocky Mountain spotted fever, which is caused by Rickettsia rickettsii. Antibodies to CTFV antigen have been detected in sera of humans in South Korea (C. Calisher, pers. comm.).- California hare coltivirus (CTFV-Ca), identified as strain S6-14-03, was isolated from the blood of the white hare, L. californicus, black-tailed jackrabbit), in northern California (outside the range of D. andersoni)ref
- Salmon River virus (SRV), which may be a serotype of both CTFV and CTFV-Ca, isolated from a person with moderately severe CTF-like illness in Idaho
,
but other ticks such as Dermacentor
occidentalis,
Dermacentor
albopictus,
Dermacentor
arumapertus,
Haemaphysalis
leporispalustris,
Otobius
lagophilus,
Ixodes
sculptus,
and Ixodes spinipalpis
are also infected with the virus. CTFV is transmitted transstadially, but
not transovarially. Infected larvae and nymphs can hibernate, and the nymphal
and adult ticks become persistently infected. In certain rodents viremia
can persist for >5 months. These ticks and rodents may provide hosts by
which the virus could overwinter. The prevalence of viremia in rodents
in a virus-endemic area ranges from 3.5% to 25%, and the prevalence in
ticks ranges from 10% to 25%ref.
CTFV has a wide host range that includes ground squirrels, chipmunks, wild
mice, wood rats, wild rabbits and hares, porcupines, marmots, deer, elk,
sheep, and coyotes. Person-to-person transmission of CTFV can occur by
blood transfusions (Philip RN, Casper EA, Cory J, Whitlock J. The potential
for transmission of arboviruses by blood transfusion with particular reference
to Colorado tick fever. In: Greenwalt J, Jamieson GA, editors. Transmissible
disease and blood transfusions. New York: Grune and Stratton; 1975. p.175–96).
This virus is included on the list of agents screened before bone marrow
transplantation in the USAref.
Prolonged viremia observed in humans and rodents is due to the intraerythrocytic
location of virions, which protects them from immune clearanceref1,
ref2,
ref3.
,
leukopenia,
arthromyalgia, nausea and
vomiting,
petechiae on limbs and maculopapular
exanthema
on trunk
(EYAV-Fr578) and Ixodes
ventalloi(EYAV-Fr577)ref.
Its antigenic relationship to CTFV was established by a complement-fixation
assayref.
Genome sequence analysis showed that CTFV and EYAV are closely relatedref
and confirmed the antigenic observations. Serologic surveys in France identified
antibodies to EYAV in 1.35% of animals, including the European rabbit (Oryctolagus
cunniculus),
mice, mountain goats, domestic goats, sheep, and deerref.
The presence of EYAV was suspected in Europe because anti-EYAV antibodies
were detected in patients with neurologic disorders. However, the natural
cycle of the virus is still unclear, and whether it circulates continuously
in Europe is not known, although the rabbit O. cunniculus is suspected
of being main hostref1,
ref2.
In 2003, the virus was reisolated from I. ricinus ticks in Germanyref
in newborns and babies
or pharyngotonsillitis)
in rotavirus-infected cells largely reduces the assembly of viroplasms
and CPE. Replication of dsRNA is partially inhibited, despite there being
no reduction in virus titre, demonstrating for the first time a key role
for NSP5 during the virus replicative cycleref.
Genome segment 11 encodes the non-structural protein NSP5 and, in some
strains, also NSP6. NSP5 is produced soon after viral infection and localizes
in cytoplasmic viroplasms, where virus replication takes place. RNA interference
by small interfering (si) RNAs targeted to genome segment 11 mRNA of 2
different strains blocked production of NSP5 in a strain-specific manner,
with a strong effect on the overall replicative cycle : inhibition of viroplasm
formation, decreased production of other structural and non-structural
proteins, synthesis of viral genomic dsRNA and production of infectious
particlesref.
after 1-4 days incubation : nausea
and vomiting,
diarrhea,
abdominal
pain,
and fever.
Dehydration (sunken eyes) is common and if not dealt with promptly has
serious consequences. Severe diarrhea and dehydration occur primarily among
children 3 months to 35 months of age. In 2 patients with rotavirus gastroenteritis
who developed encephalopathy, rotavirus RNA was detected in the cerebrospinal
fluid (CSF) by RT-PCR; in 1 patient, rotavirus RNA was detected on 2 occasions
3 weeks apart. There are increasing reports of cases in which patients
who have seizures after an episode of rotavirus diarrhea have evidence
of rotavirus in their CSF. A search of 2 large hospital discharge databases
suggested that seizures are noted as part of the discharge diagnosis in
the records of, at most, <4% of patients with rotavirus diarrhea versus
7% of patients with bacterial diarrhea. Although evidence suggesting that
rotavirus is a cause of central nervous system sequelae remains inconclusive,
the 2 case reports presented in this study further illustrate a possible
association. Further study is required to determine whether detection of
rotavirus in CSF represents a true pathogen, CSF contamination that occurs
at the time of lumbar puncture or in the laboratory, or carriage of rotavirus
RNA in trafficking lymphocytesref
: a case of rotavirus cerebellitis
was reportedref
for rotavirus. Efforts to develop an effective and safe vaccine resulted
in licensing in 1998 of a live oral vaccine (RotaShield) that was withdrawn
less than one year later, after 9 reports of intussusception occurred within
the 1st 7 months of vaccine use, more than double the cases reported in
the previous 7 years. Intussusception occurs when the intestine telescopes
into itself, causing an obstruction of the bowel that may have to be repaired
surgically. An investigation of vaccinated infants confirmed that the vaccine
was indeed the cause of the complication. Most of these infants had intussusception
shortly after their vaccination. The risk of intussusception was 10 times
higher than normal, and within the 1st 7 days after vaccination, the risk
was 14 times higher than normal. This experience with RotaShield has resulted
in the development of new candidate rotavirus vaccines that are currently
in late phase III clinical trials. One of these vaccines, GlaxoSmithKline's
Rotarix, was licensed in July 2004 to be used in Mexicoref.
,
Culex
fuscocephala,
Anopheles
vagus,
Anopheles
aconitus,
Anopheles
subpictus,
and Aedes dorsalis.
Seadornaviruses were shown to replicate in adult laboratory mice and were
detected in infected mouse blood at 3 days postinfection until day 5 postinfectionref.
upregulation, an innate immune response against invading pathogens that
could help the host clear infection effectivelyref
(multimammate mouse : usually without obvious signs of disease)
prophylaxis was not recommended for persons who might have been exposed
to the patient described in this report. Instead, a standard treatment
regimen of intravenous ribavirin was recommended for any contacts with
clinical evidence of infection during the incubation period. Because of
the serious nature of the disease, vigilance is required in assessment
and treatment of patients arriving with febrile symptoms from endemic areas.
(lasting for 7-17 days), malaise, headache,
and abdominal pain.
Other symptoms are conjunctivitis,
facial edema, pharyngitis, dry cough,
retrosternal pain, nausea
and vomiting,
diarrhea,
back pain, myalgia, and occasionally a maculopapular
exanthema.
Respiratory and pulse rates and temperature are increased and blood pressure
decreased. Neurological symptoms may also occur, including sensorineuraldeafness
(25-30% : may be permanent),
tremors, and encephalitis
,
peripheral vasoconstriction, hypovolemia, and anuria
.
.
.
)
is the primary reservoir for LCMV, with a prevalence of infection of 3-40%;
a high degree of focality often is notedref1,
ref2,
ref3))
:
for 8-10 days : lethal in immunosoppressed patients or self-limiting within
15-20 daysref
in Colombia, and isolated from human subclinical infections.,
Sigmodon
hispidus
and Oryzomys spp.).
After 7-16 days incubation : fever,
chills, myalgia, nausea and
vomiting,
generalized lymphadenitis,
shock, oligoanuria, DIC,
hemorrhages, neurological disorders => death (5-30%)
and Calomys musculinus).
After 7-16 days incubation : high fever,
chills, leukopenia,thrombocytopenia,
generalized myalgia, nausea
and vomiting,
generalized lymphadenitis,
exanthema, shock, oligoanuria, DIC,
hemorrhages, neurological disorders => death (5-30%)
: virus causes persistent infection of its rodent host accompanied by abundant
shedding of virus in urine, saliva and feces, which are the sources of
infection for rodents and humans alike. In its natural host, Machupo virus
eventually causes hemolytic anaemia as well as fetal death) with interhuman
transmission, too
,
chills, myalgia, nausea and
vomiting,
generalized lymphadenitis,
shock, oligoanuria, DIC,
hemorrhages, neurological disorders => death (5-30% in untreated cases).
It is considered by CDC as a category A biological
weapon
,
chills, myalgia, nausea and
vomiting,
generalized lymphadenitis,
shock, oligoanuria, DIC,
hemorrhages, neurological disorders => death (5-30%).
and Argas hermanni).
It is ether-sensitive and presumed to contain RNA.
Viral person-to-person transmission of ANDV Sout lineage was described
for the first time during an HPS outbreak due to ANDV Sout lineage in southwest
Argentina in 1996, in which 16 persons were involvedref1,
ref2,
ref3,
but in general, clusters of HPS cases are mainly attributed to a common
source of rodent exposure. This mechanism of interhuman virus spread, which
makes ANDV unique among the hantaviruses, is not the only exclusive feature
of this virus. ANDV was the only American hantavirus isolated from human
serumref.
Most importantly, ANDV was shown to be highly lethal in Syrian hamsters,
and the characteristics of the disease closely resembled HPS in humansref.
Similar results have been recently obtained with Maporal virusref
and ANDV Cent BsAsref.
It occurs during the prodromal phase or shortly after it ends
.
In contrast to mechanical ventilation, which is available at any referral
center, ECMO offers the distinct advantage of supporting patients whose
cardiac function is markedly impaired by disease, as is almost universal
in patients with severe "HPS". The intensive care unit physicians hoped
that the adoption of the nomenclature "hantavirus cardiopulmonary syndrome"
would improve the understanding among referring physicians of the importance
of providing cardiac support for patients with HCPS. This hope may be justified,
as referring physicians appear to be more aware of the cardiac manifestations
of HCPS in the wake of the use of the term by referral center providers.
In the case of Andes virus infection, renal insufficiency and muscle inflammation
are observed more frequently than is the case with Sin Nombre virus infection
in North America
in Panama
in northern Colombia
ref
and Apodemus sylvaticus)
(virus isolates obtained from two of these rodents were the first successful
isolations of a pathogenic South American hantavirus. Analysis of the prototype
LN virus entire S and M and partial L segment nucleotide and deduced amino
acid sequences showed that this virus is unique member of the Sigmodontinae-borne
clade of hantavirusesref)
in northern Colombia
droppings
,
hemoconcentration, and thrombocytopenia;
bilateral pulmonary interstitial infiltrates are seen on x-ray
.
and Rattus rattus)
with the onset of colder weather => indirect infection of humans occurs
by inhalation of rodent detritus and rarely faecal contamination of food
,headache,
photophobia,
blurred vision, prostration, nausea
and vomiting,
facial
flushing extending to neck and shoulders, conjunctival petechiae, periorbital
edema,
acute
pharyngitis,
axillary petechiae, lumbar back pain and CVA tenderness lasting 3-5 days.
The illness may gradually resolve after this febrile stage or a systemic
arterial hypotension
stage may begin as the temperature falls. The hypotensive stage is characterized
by decreased blood pressure, tachycardia, and sometimes shock. Proteinuria,
thrombocytopenia,
leukocytosis,
and acute
renal failure
occur in some cases. Renal function returns as the oliguric phase resolves
and the polyuric phase ensues. Electrolyte imbalances and dehydration may
occur in the polyuric phase. Disseminated intravascular coagulation may
occur relatively early in the course of illness.
.
HFRS cases are usually coincident with invasion of human dwellings by field
and forest rodents with the onset of colder weather. Indirect infection
of humans occurs by inhalation of rodent detritus, although some outbreaks
have been related to fecal contamination of food supplies.
,
a milder form of HFRS than that caused by Hantaan virus : 10-25 days incubation
=> fever,
oliguria => polyuria and hydroelectrolytical disequilibrium after recovery.
(bank vole), Clethrionomys
rufocanus,
and Clethrionomys
rutilus.
HFRS is endemic in the Republic of Tatarstan. Public health authorities
in Russia reported in April 2005 that the incidence of rodentborne HFRS
nationwide during 2004 was 66.4% higher than the 2003 level, with a 180%
increase reported among children under the age of 14. These new national
statistics followed previous announcements of a 13-fold increase in the
incidence of HFRS in Nizhnii Novgorod and a 21-fold increase in Sverdlovsk
during 2004. 10 244 cases of HFRS -- including 377 cases in children under
age 14 -- were reported from Russia in 2004. The national rate of HFRS
incidence for 2004 was cited as 7.1 per 100 000 inhabitants, whereas in
2003 it was 4.3. The general incidence rose by 66.4%, including a 2.8-fold
rise among children under age 14. Rates of HFRS transmission in Sverdlovsk
Oblast were 21 times higher in 2004 than during 2003, and > 8 times higher
than the running average for the region over the past several years. Rates
of infection for tularemia in Russia as a whole were reported to be 3 times
higher during the 1st 9 months of 2004 than they were in 2003ref.
The reported massive increases in animalborne diseases are attributable
to a combination of breakdowns in vaccination and rodent control programs
at the local and provincial levels due to reduced government funding levels
and massive increases in population densities of disease-carrying rodents.
Officials attributed an observed 6-fold increase in the number of fox-transmitted
rabies incidents among humans in Sverdlovsk Oblast during January 2005
over 2004 levels to unusually high survivorship rates of young foxes permitted
by recent population explosions among their usual prey species: rodents,
rabbits, and other small mammals. The highest number of HFRS cases in 2004
was recorded in the Privolzhskiy Federal District -- 28.2 per 100 000 inhabitants,
4 times the average for Russia as a whole. In 2004 in Mariy El Republic
HFRS morbidity was 53.2 per 100 000 inhabitantsref
: in total 387 cases of HFRS, 4 of which had a fatal outcome, were recorded
in Mariy El in 2004
(transovarial and transstadial transmission))
and small mammals, whereas adult ticks attack larger wild and domestic
ruminants like Ovis
aries,
Capra
hircus
and Bos taurus).
Infection of wild and domestic ruminants results in abundant production
of CCHFV. Remarkably, there is no evidence of clinical disease in animals
other than humans
and myalgia, headache,
dizziness,
photophobia,
hyperesthesias, chest, back and/or abdominal
pain,
nausea
and vomiting,
conjunctivitis,
flushing, systemic
arterial hypotension,
axillary or other petechiae, systemic
arterial hypotension,
tachycardia, periorbital edema, proteinuria, acute
hepatitis,
jaundice,
hepatomegaly,
elevated serum levels of liver enzymes (AST, CPK), leukocytosis,
and DIC
after several days of infection. Death usually occurs during the second
week of illness, preceded by hemorrhages, shock, pulmonary edema and acute
renal failure.
,
surgical stemming of internal hemorrhage and blood transfusion.
and goats, causes disease in humans, and is widespread throughout East
Africa. Ganjam virus has caused disease in goats and humans in India. Due
to their occurrence on different continents and association with different
ticks, these viruses were considered distinct despite serologic cross-reactivity.
Their S RNA genome segments and encoded nucleocapsid proteins were found
to be 1590 nucleotides and 482 amino acids in length and differed by only
10 and 3% at nucleotide and amino acid levels, respectively. Genetic and
serologic data demonstrate that Ganjam virus is an Asian variant of NSD
virus. These viruses were phylogenetically more closely related to Hazara
virus than Dugbe virus.
)
,
Anopheles
spp.,
and Aedes spp.),
most frequently from Anopheles quadrimaculatusref,
the principal mosquito vectors are unknown. The vertebrate amplifying hosts
of CVV have been little studied, but a high prevalance of neutralizing
antibody to this virus is often found in ungulatesref,
including deer, sheep, horses, and cattleref1,
ref2,
ref3.
The virus has been isolated from a healthy cow and a sick sheep in Texasref
and from a healthy horse in Michiganref.
It is teratogenic in sheepref.
Mutual exclusion with Tensaw virus likely occurs
because of cross-protectivity between them
in a young adult in North Carolina in 1995ref
in a a 41-year-old man in October 2003 who recoveredref
and Aedes spp.;
mutual exclusion with Cache Valley virus
likely occurs because of cross-protectivity between them
and headache
,
and monkeys; human infection is asymptomatic
; vectors : Aedes atlanticus,
Aedes
infirmatus,
Culex
tarsalis,
Aedes
melanimon
ref1,
ref2,
a mosquito of woodlands, and small mammals such as chipmunks and squirrels.
These small mammals may become sufficiently viremic to infect hematophagous
mosquitoes
.
The incubation period is about one week, followed by a non-specific febrile
period and an acute encephalitis which may last up to 10 days. Although
there may be persistent disabilities in a minority of cases, fatalities
are rare
,
sometimes associated with acute
pharyngitis,
lung symptoms and aseptical meningitis.,
muscular and articular pains, and occasionally nausea and vertigo.
and Coquillettidia venezuelensis
,
chills, malaise, headache,
myalgia, and arthralgia, sometimes with nausea and nausea
and vomiting,
and occasionally with aseptical meningitis
and Eretmapoditeschrysogaster
in Africa; serologically related species infect humans and other animals,
and pains of localized and generalized distribution, in Panama.,
Capra
hircus,
and Bos taurus
(abortions in pregnant animals and a high mortality rate in the newborn),
transovarial transmission in Aedes
mcintoshi,
rodents.,
Aedes caballus,
Aedes
circumluteolus,
Aedes
vexans arabiensis,
Culex
theilesi,
Culex
pipiens,
Culex
fatigans,
Culex
tritaeniorhyncus,
Mansonia
spp.,
Eretmapoditeschrysogaster.
In massive numbers, Phlebotomus
spp.,
Simulium
spp.,
Glossina
morsitans,
and Culicoides spp.
may mechanically spread RVFV.,
chills,
headache,
myalgia, weakness, diarrhea,
nausea
and vomiting,
and hemorrhages, back pain, dizziness,
and rapid weight loss lasting 4 to 6 days with slow recovery. Retinal
vasculitis occurs in about 10% of cases,
and acute meningoencephalitis
(CFR = 10%)
.,
TOSV was first isolated in Italy from the sandfly Phlebotomus
perniciosus
and later from Phlebotomus
perfiliewiref
(Verani P, Lopes MC, Nicoletti L, Balducci M. Studies on phlebotomus-transmitted
viruses in Italy. Isolation and characterization of a sandfly fever Naples-like
virus. In: Vesenjak-Hirjan J, Porterfield JS, Arslanagic E, editors. Arboviruses
in the Mediterranean countries. Stuttgart: Gustav Fischer Verlag; 1980.
p. 195–201). P. perniciosus is the most abundant anthropophilic
species of Phlebotomus in Spain (Gil-Collado J, Morillas-Márquez
F, Sanchis-Marín MC. Los flebotomos en España. Revista de
Sanidad e Higiene Publica. 1989;63:15–34). The maximum activity of sandfly
vectors for TOSV occurs during summer, along with most cases of TOSV infectionref
,
headache,
myalgia; rarely acute aseptic meningitis
and meningoencephalitis.
Although TOSV is not normally associated with mild disease, serologic studies
report high seroprevalence rates in areas of confirmed TOSV infectionsref1,
ref2,
ref3.
Furthermore, a case of influenza-like illness caused by TOSV has recently
been reportedref.
The high seroprevalence rates suggest that the diagnosis of TOSV infection
is frequently missed since most cases are mild, as occurs with SFSV and
SFNV infectionsref,
a severe illness involving the central nervous system develops in only
a few patients. Despite this, fewer cases of severe disease caused by TOSV
occur in Granada arearef
than in other countriesref.
A possible explanation for this could be that Spanish TOSV are less neurovirulent
than the Italian. Whether changes in other parts of the genome, such as
the noncoding regions, affect the neurovirulence of this virus, as described
for tickborne encephalitis virusref,
needs to be investigatedref
,
erythema on face and trunk, headache,
myalgia, rarely meningitis
disease occurring chiefly during the warm months in parts of the Mediterranean
littoral, central Asia, the Middle East, and Central and South America.
It is caused by any of several types of Phlebovirus and transmitted by
the urban sandfly Phlebotomus
papatasi,
except in the Americas, where the vectors are sylvan sandflies Lutzomyiaspp.)
droppings.
that rapidly progresses to shock and acute
respiratory distress syndrome (ARDS)
with thrombocytopenia,
hemoconcentration, hemorrhages and leukocytosis
and Ovis
aries,
although many animals can be infected experimentallyref1,
ref2,
ref3.
In northern regions, they often live in gardens, outhouses, and farm buildings,
and in the Alps, they can be found <1,600 m above sea level. Shrews
are carnivores, and their diet consists of insects and snails, but they
may also eat forageref.
They live on the ground and do not climb, which could explain why mainly
horses (during the grazing season) or animals located in old-fashioned
farmhouses without feeding troughs are affected by BD. BD shows an increased
incidence in spring and (early) summer, when most shrews are found in pastures
and in close contact with grazing animals. In winter, some species of the
genus Crocidura show social acceptance and group together, which may be
a possible source of infection between shrewsref.
In an experimental study by Sauder and Staeheliref,
rats persistently infected with BDV and naive rats were put together, which
led to infection of the naive rats after cohabitation. Most animals showed
signs of disease 5–6 weeks after first contact with carrier rats, and high
virus titers were found in their urine.
)
inclusion bodies can be observedref1,
ref2.
The nucleoprotein (p38/40, open reading frame [ORF] I) and the phosphoprotein
(p24, ORF II) are the 2 most important BDV target proteins and genes for
IHC, RT-PCR, and TaqMan real-time RT-PCR, respectivelyref1,
ref2,
ref3,
ref4,
ref5,
ref6,
ref7
,
expecially Gallus gallus
(see veterinary
medicine).
Infected people will shed the virus in secretions for a period of time
after exposure
and malaise
(sporadically expressed by neural cells) for entry. That virus could enter
the CNS either by direct infection of endothelial cells or in infected
leucocytes, followed by infection of predominately neurons and oligodendrocytes.
in babies
and acute bronchitisin
babies
in immunocompromised patients
in babies
,
humidification by air and inhalation of epinephrine, ribavirin.,
acute
pharyngitis,
acute
bronchitis,
usually being accompanied by fever.
epidemics among recruits
.
Routine immunization with mumps virus was introduced in 1968. During 1990
to 2001, infant vaccine coverage ranged from 85-92% :,
monolateral
parotitis
(60-75%, evolving to bilateral within 1-5 days; Tresilian's sign
: a reddish appearance in Stensen's duct; Hatchcock's sign : tenderness
on running the finger toward the angle of the jaw in mumps).
(10%), self-limiting within 5-10 days.
(1 case in 6,000) : 50% lethality
(20% of males after puberty; bilateral in 25%) self-limiting within 5-7
days with some degree of testicular atrophy (some bilateral forms can undergo
fibrosis and result in permanent sterility).
(self-limiting in 5-6 days : 15 days for pancreatitis necroticans)
in newborn
(in pregnants infected in the first quarter of pregnancy)
within 2 weeks since healing (self-limiting).
A serosurvey for prevalence of mumps antibodies in Europe (Denmark, England
and wales, France, Germany, Italy and The Netherlands) as part of the European
Sero-Epidemiology network (ESEN) concluded that a build-up of susceptibles
in older children and adolescents in England and Wales, France, the former
West Germany and Italy indicates the possibility of further mumps outbreaks
in secondary school environmentsref.
A serologic study done in Spain showed a vaccine efficacy of 76.7% in children
2-5 years of age felt to be associated with use of the Rubini vaccine strainref.
An earlier study of mumps vaccine efficacy during an outbreak in Spain
showed a one dose vaccine efficacy of 46% (range 0-84%) and a 2 dose efficacy
of 87% (range 27-99)ref.
A study compared vaccine efficacy of 3 different mumps vaccine strains
in Switzerland during a mumps outbreak where they observed a similar attack
rate in unvaccinated children (63%) and children vaccinated with the Rubini
strain (67%) but significantly lower in those vaccinated with the Jeryl-Lynn
(14%) or the Urabe strain (8%). The comparative vaccine efficacies were
minus 4% (range minus 218 to 15%) for the Rubini strain, 78% (range
64 to 82%) for the Jeryl-Lynn strain, and 87% (76-94%)ref.
and interstitial
pneumonia
in children (around age 7) : around 12% of archived blood samples from
under-5 with respiratory illness test positive for hMPV (second only to
RSV, which accounts for 50% of illness). hMPV may account for 10% of elderly
patients hospitalized with respiratory infections, compared to 12% for
flu. Re-infections are far less severe;
direct contact with RSV F is necessary and sufficient to inhibit proliferation
of PBLsref
responseref1,
ref2,
ref3.
A delayed Th1 response seems also to be an important factor
in measles virus-mediated
immune suppression and appears to be triggered by deteriorated cytokine
secretion by infected macrophages and lymphocytesref.
Inhibition of lymphocyte proliferation by RSV was previously attributed
solely to effects caused by virus replication in lymphocytes and to cytokines
secreted from infected cells. Infection of macrophages and lymphocytes
with BRSV and HRSV has been demonstrated both in vitro and in
vivoref1,
ref2,
ref3,
ref4,
ref5.
In vitro, RSV infection of peripheral blood mononuclear cells (PBMCs)
was reported to result in suppression or delay of proliferation of PBMCs
after stimulation with phytohemagglutinin (PHA) or with EBV antigen. Production
of cytokines such as IFN-g and IL-1 inhibitor
was considered responsible for the observed inhibition of PBMC proliferationref1,
ref2,
ref3
before age 2 : infants may have recurrent wheezing and asthma later in
childhood.
throughout the USA, Canada, and Mexico. It is not known to be associated
with any animal, or human, disease
insectivorous bat which had been caught in daylight by a cat in Makhado
town (formerly Louis Trichardt) in Limpopo province, about 250 km to the
north of the present incident, and in 1986, the virus was obtained from
an insectivorous bat, Nycteris
thebaica,
caught near a mine shaft across the border from Limpopo province in Zimbabwe.
Since 1981, there have been several isolations of another rabies-related
virus, Lagos bat virus, from fruit bats in KwaZulu-Natal province of South
Africa, but the virus has never been associated with human disease. There
have also been several isolations of the rabies-related Mokola virus from
cats with rabies-like disease in KwaZulu-Natal and Eastern Cape provinces
of South Africa. Mokola virus is ostensibly associated with shrews and
rodents, not bats, and it was isolated from 2 human patients with nervous
disease in 1969 and 1971, shortly after its initial discovery in Nigeria
in 1968. Widely distributed in bats in Europe and Africa. In 2006 a case
involved a 77-year-old man who was scratched on the face by what appears
to have been an insectivorous bat in February 2006 in North West Province,
South Africa, about 80 km from the original incident : he became sick one
month later, and died on day 14 of illness.
).
Between 1977 and 2000, 620 cases of EBLV-1 infection in bats were reported
in a number of countries including Denmark, France, Germany, the Netherlands,
Spain and UK : >95% of viral isolates diagnosed have been confirmed as
EBLV-1. EBLV infection in bats may include full recovery with sterilizing
immunity.
on May 30 1996 from the cellar of a public house in Newhaven, East Sussexref1,
ref2,
September 2002ref1,
ref2,
ref3and
203, ref2
in Lancashire, and September 2004 in Staines, Surrey, southern Englandref1,
ref2.
Surveys carried out of captured free-living bats in Scotland and the north
and south of England have found EBLV-2 antibodies in but no virus
has been isolatedref1,
ref2.
This suggests that some species of bat may be adapted to the virus and
able to recover from infection and become non-infectious. Daubenton's bats
do not tend to live near or in human habitations. Pipistrelle bats, one
of the more common species, often roost in houses, ut the virus has never
been isolated from this species in the UK
,
which are not found in the UK) and Myotis
daubentoniiref1,
ref2,
ref3
(prevalence of antibodies = 4-15%, but so far all oral saliva swabs tested
by RT-PCR have been negative, giving rise to the possibility that bats
could be seropositive without excreting virus in saliva. Improved sampling
methods will be employed in future to determine whether bats are clinically
silent carriers of virus with only intermittent secretion of virus in saliva
or whether they recover completely from a self-limiting infectionref1,
ref2)
,
Aedes
spp.
& Culex spp.
have transmitted it in the laboratory. Antibodies have been found in livestock
& rhesus Macaca mulatta,
suggesting they may be reservoir hosts
=> loss of consciousness that deteriorates to a deep coma and decerebrate
posturing
,
with gross brain edema, but there are important differences. The site of
the lesion was the area supplied by the middle cerebral artery. There was
no clinical evidence of invasion by a pathogen. The nature of the arterial
pathology is likely to be spasm or transient obstruction due to vasculitis,
rather than thromboembolism. That such a disease could arise as an epidemic
is new information. If Chandipura virus is the cause, the disease is mediated
via vasculitis, not encephalitis. Otherwise another infectious agent, probably
viral, might be involved. Infection is invoked to explain an epidemic.
Outbreaks of acute encephalopathy with high case fatality reminiscent of
this outbreak have been reported repeatedly in several northern Indian
towns and villagesref.
To assume an illness is infectious just because it affects a group of people
could be misleading. Sriramachariref
has suggested the clinical features of the recurrent encephalopathy outbreaks
in northern India could be due to high environmental temperature, with
or without secondary factors. He believes that the heat-related encephalopathy
has all the brain features of Reye's syndrome. B Rao and colleaguesref
note that the summer temperature in the outbreak region was 36-49°C.
Both reportsref
state that fever was a consistent feature. Some children indeed had hyperpyrexiaref.
Cases were widely scattered. The subject is well worth further researchref.
and blackflies from the family Simuliidae.
The disease occurs sporadically, but outbreaks generally follow a 10--15-year
cycle
,
Bos
taurus,
and Equus
caballus;
occasionally Capra hircus,
Cervidae
and Ovis
aries
; vectors : sand flies and black flies. Infected animals with open sores
can expose herd mates to the disease through close contact or by the sharing
of feed buckets or bits. As a precaution, all infected and susceptible
livestock on a premise are quarantined until at least 30 days after all
infected animals have healed.
)
and on the dental pad, tongue, lips, nostrils, hooves, and teats. These
blisters swell and break, leaving raw tissue that is so painful that infected
animals generally refuse to eat and drink and show signs of lameness. Severe
weight loss usually follows, and in dairy cows, a severe drop in milk production
commonly occurs. Affected dairy cattle can appear to be normal and will
continue to eat about half of their feed intake. There may also be vesicles
in swine on the snout and interdigital spaces, in cattle on the udder and
teats, and in horses on the coronary bandref.
It must be distinguished from foot-and-mouth
disease, which doesn't affect horses.
and influenza B virus) molecules of linear negative-sense single-stranded
RNA (total MW approximately 5 x 106, total size 10.0–13.6
kb). Viruses contain 7-9 major polypeptides, including a transcriptase
and a neuramidase, and are sensitive to lipid solvents, radiation, and
disinfectants. Replication occurs in the nucleus and cytoplasm, and assembly
is by budding on the plasma membrane. There are 3 genera, each represented
by single virus species.)
and epiglottitis
has been reported in up to 25% of children in some influenza B outbreaks
(when administered within 48 hours of symptom onset, antiviral treatment
of influenza can reduce the duration of illness by approximately 1 day
in healthy adults. Data on the use of any of the 4 antiviral agents during
pregnancy are not available)
and subunit
vaccines. The composition of the vaccine is changed each year in response
to antigenic shifts and changes in prevalence of influenza virus strains;
the vaccine is usually bivalent or trivalent, containing 1-2 influenza
virus A strains and 1 influenza virus B strain. Annual immunization before
November is recommended for high-risk individuals (persons over 65 years
of age and persons with chronic disease). The last time the vaccine missed
the mark was in 1997, when the strain A-Sydney appeared that was significantly
different from the strain included in the flu shot, which remained just
30-50% protective.
in China, but these viruses are not associated with either epidemic or
pandemic disease in the human population.They appear to be antigenically
stable and cause only sporadic disease
,
and Ovis
aries
in Africa
and optic neuritis
after 24-72 hours incubation
was high (sharing toilet facilities and restrooms)ref1,
ref2,ref3;
asymptomatic cases have been reported to have helped spread outbreaksref;
the difficulty of controlling person-to-person spread has been documented,
especially if symptoms include vomitingref
("winter vomiting
disease") : after 16-48 hours incubation => nausea
and vomiting,
diarrhea
and fever
lasting 12-48 hours.
-dependent
innate immunity, but not T and B cell-dependent adaptive immunity, is essential
for resistance to murine norovirus 1 infection in mice (which anyway do
not suffer gastrointestinal problems)ref
after 24-72 hours incubation
of viral infection.
and Aedes
albopictus
are known vectors of dengue in China, with the former species being regarded
as the more efficient. However, Ae. aegypti is mainly restricted
to coastal areas south of a latitude of about 22°, while Ae.
albopictus has a more widespread distribution and appears to be the
main vector in inland localities. But in some areas both species can be
vectors, such as on Hainan island. Although there is no information on
the vector in the city of Cixi, Zhejiang, if local transmission was responsible
for the recorded dengue cases then it would appear that the vector might
be Ae. albopictus. However, more information is needed on any vector
identification made by the authorities in Cixi, and what anti-mosquito
control operations, if any, were employed,
Aedes
albopictus,Aedes
scutellaris,
Aedes
polynesiensis
(it is true that in West Africa isolates of dengue virus have been obtained
from Aedesafricanus
and a few other forest mosquitoes, but any role they play is likely to
involve monkey transmission in enzootic forest cycles) which become infectious
since 8-10 days from feeding on an infected human for life
: a 23-year-old male with ESRF due to lupus nephritis underwent a living
donor renal transplantation. The donor was his mother, who was healthy
except for a past history of dengue fever 6 months previously. At posttransplantation
day 5 blood RT-PCRwas positive for dengue virus serotype 1. Over the next
week, he continued to spike high temperatures with a fall in platelet count
and a deterioration of his general clinical condition. On the 12th post-operative
day, he developed upper gastrointestinal bleeding, gross hematuria and
tachycardia. On the 15th post-operative day, he complained of left side
pain and abdominal distension. CT of his abdomen revealed a large retroperitoneal
hematoma arising from the bed of the transplanted kidney. Emergency laparotomy
was undertaken for surgical hemostasis and evacuation of the hematoma.
There was a perforation seen in the peritoneum, which allowed communication
between the retroperitoneal and intraperitoneal spaces. The transplanted
kidney appeared healthy. A repeat dengue RT-PCR was negative. Post-operative
recovery was uneventful, with resolution of fever and recovery of thrombocytopenia
within the next week. Hemorrhagic tendencies ceased spontaneously with
resolution of hemetemesis and hematuria. His graft function remained excellent.
The pathophysiological mechanisms underlying DHF remains controversial.
There is strong evidence to suggest an increased risk of DHF with secondary
dengue virus infection. The presence of pre-existing anti-dengue antibodies
increases viremia titres by a phenomenon known as ADE. Having lived in
a dengue-endemic region, the patient may have been infected previously
but was asymptomatic or had subclinical infection. 45% of the adult population
in Singapore is seropositive for dengue. Transplantation of the dengue-infected
allograft can cause secondary infection and development of DHF. It is not
known whether donor organs remain infected after apparent resolution of
viremia. Alternatively, secondary transmission could have been via the
usual route, the bite of a mosquito. However, there was no active transmission
of dengue in our area during this period, making hospital-acquired infection
less likely. Clinical presentation and course of the illness in this immunosuppressed
patient is similar to that in the immunocompetent, except for a longer
period of illness. The patient experienced a prolonged course of illness
(19 days) as well as prolonged duration of thrombocytopenia (12 days).
The mean duration of illness is 2-7 days and duration of thrombocytopenia
3.6 days (±1.6 days). The critical stage in DHF is usually around
the time of defervescence, with circulatory failure of hemorrhagic manifestations
occurring about 24 h before to 24 h after the temperature falls to normal
or below. DHF occurring early post-operatively poses a potential danger
to the transplant patient. Bleeding diathesis resulting from thrombocytopenia,
dysfunctional surviving platelets and increased fibrinolysis result in
persistent hemorrhage especially from cut tissue surfaces. Hypovolemia
poses a risk of damage to the allograft. Hypoalbuminemia secondary to leakage
of plasma aggravates the problem of poor wound healing in the immunosuppressed
transplant recipient. No specific therapy or vaccine exists for DHF. Management
is supportive, with correction of hypovolemia and coagulation abnormalities.
Screening donors of organs and blood products may be beneficial, although
sensitivity, feasibility and cost benefits of screening need to be assessedref.
with chills for up to a week with >= 2 of the following: headache,
nausea
and vomiting,
abdominal pain, severe myalgia and arthralgia (hence breakbone fever),
morbilliform
or scarlatiniform
maculopapular exanthema (in the abdomen area, thereafter
reaching the face and limbs).
Also
facial flushing, lumbosacral aching pain, acute
hepatitis,
conjunctivitis,
changes in taste, sore throat => diarrhea,
anorexia,
and depression. May have positive tourniquet test result and/or spontaneous
bleeding (e.g., skin petechiae, bruising, mucosal/gastrointestinal bleeding).
Not apparently increased vascular permeability. Maximum hematocrit <44%.
Thrombocytopenia may be present. Usually self-limiting.
for 2-7 days, DIC
due to type II hypersensitivity (NS1 protein cross-reacts with human endothelial
cells inducing apoptosis), myocarditis
and various neurologic disorders due to meningoencephalitis.
During acute infection, up to 7% of circulating CD8+ T cells
react with the A11-restricted GTS epitope, and there was an association
between the magnitude of the T-cell response and the disease severity.
Most of the CD8+ T cells present show an activated phenotype
and undergo PCD. In addition, many dengue-specific T cells are of low affinity
for the infecting virus and show higher affinity for other, probably previously
encountered strains. Must have positive tourniquet test result and/or spontaneous
bleeding. DHF is characterized by fever, minor or major bleeding
manifestations, thrombocytopenia (<100 000 platelets/mL),
and evidence of increased vascular permeability (e.g., hemoconcentration
[hematocrit >20% higher than baseline or >=
44%], pleural or abdominal effusions, or hypoproteinemia)ref.
The
WHO distinguishes 4 types according to severity :
and Sus scrofa
(causing significant mortality and morbidity); terminal host : Equus
caballus;
vectors are > 28 mosquito species, most being in the genus Culex
(transovarial
transmission in Culex
tritaeniorhyncus
(a species that breeds in rice fields and is found in most parts of Asia,
including Hong Kong), Culex
gelidus,
Culex
vishnui
(both of which are present in Hong Kong), Culex
fuscocephala),
but also others in the genera
Aedes
(Aedes
aegypti),
Mansonia,Armigeres,
and Anopheles
spp.
(which breed in rice fields). All these vectors commonly breed in rice
fields, but they can also be found in other types of larval habitats such
as in marshes, pools of water, especially those formed adjacent to streams,
and hence their larval habitats can extend to urban or semi-urban areasThe
virus is transmitted in an enzootic cycle among mosquitoes and vertebrate-
amplifying hosts, chiefly domestic pigs and Ardeid (wading) birds (Burke
DS, Leake CJ. Japanese encephalitis. In: Monath TP, ed. The arboviruses:
epidemiology and ecology, Vol 3. Boca Raton, FL: CRC Press, 1988:63-92).
Viral infection rates in the mosquitoes range from < 1 to 3%. These
species are prolific in rural areas, where their larvae breed in ground
pools and especially in flooded rice fields.
with cortical damage and cord lesions resembling those of poliomyelitis)
(1/300 : 1 in 20 to 1,000). Lethality < 10%, but children aged <
15 years are particularly at risk and mortality in them may reach 30%;
severe neuropsychical sequelae in 30-70% of patients who recoverref
(Halstead SB. Arboviruses of the Pacific and Southeast Asia. In: Feigin
RD and Cherry JD, eds. Textbook of pediatric infectious diseases,
third edition. Philadelphia, PA: WB Saunders, 1992:1468-75)
and attenuated
vaccines against type B are available and have been used widely in mainland
China.
,
Aedes
camptorhynchus
and
Culex annulirostris
;
vectors : Culex annulirostris,
Culex
australicus,
Culex
bitaeniorhynchus,
Culex
fatigans,
Culex
pipiens quinquefasciatus,
Aedes
aegypti,
Aedes
camptorhynchus,
Aedes
eidsvoldensis,
Aedes
normanensis,
Aedes
notoscriptus,
Aedes
sagax,
Aedes
theobaldi,
Mansonia
spp.
of viral infection.
(MVE) (lethality : 50%)
(wild passeriform and columbiform birds)-mosquito cycle, with periodic
amplification in peridomestic birds and culicine mosquitoes. The principal
vector in the south-east is Culex
nigripalpus,
in the midwest Culex
pipiens pipiens,
and in the west Culex tarsalis,
Culex
neavei,
and
),
birds, and mammals
; feverwith
rash in humans; there have been no reports of severe disease in humans.
may be hosts. It is related to St.
Louis encephalitis virus, Japanese
B encephalitis virus, and West Nile
virus
and bizarre neurological manifestationsin
laboratory workers)
or bites of an infected tick or orally by drinking unpasteurized contaminated
Camelidae
meat and milk. Alkhurma virus cases are usually detected
around the time of the Hajj (when pilgrims visit the holy city of Mecca)
because there is increased animal movement and slaughtering. Increased
slaughtering of animals and animal movement does not necessarily mean increased
risks to pilgrims visiting Makkah [Mecca] : greatest risk occurs when pilgrims
slaughter animals themselves or there is other direct contact with animals.
The Saudi Government greatly minimizes this risk by providing for pilgrims
a proxy service that takes care of all animal slaughtering, butchering,
and distribution. Payment is made at banks and kiosks remotely located
from the slaughter sites. Most of the pilgrims from the West do make use
of this facility. The virus is very stable and can be isolated from serum
samples kept in the lab in an ordinary domestic refrigerator for about
1 year. This means that infected sheep meat kept in a domestic freezer
could still transmit the virus to housewives preparing the meat if their
hands had cuts and abrasions.
rather than encephalitis
: nausea and vomiting
=> fever, confusion, leucopenia, thrombocytopenia,
impaired renal function with elevated creatinine, elevated AST, progressive
systemic
arterial hypotension,
bleeding, and cardiac arrest.
)
and the red faced bonnet macaque (Macaca
radiata)),
macaques (Macaca radiata),
shrews (Suncus murinus),
rats (Rattus wroughtoni),
Aves
spp.,
squirrels, and bats;
vector : unfed nymphs of Haemaphysalis
spinigera.
The disease is known to thrive under prolonged periods of dryness. The
appearance of dead monkeys in the endemic area may herald an epidemic
and severe headache,
followed by back and extremity pain, bradycardia, lymphadenitis,
conjunctivitis,
palantine injection, petechiae, bleeding from the nose and throat. Meningoencephalitis
is relatively common
is available for protection of those at risk and for post-exposure treatment
to moderate the course of illness; controlling the tick population by chemical
spraying; and personal protection by using insect repellents on clothing.
88,152
people in an endemic area were vaccinated during 1990 to 1992. Epidemics
of KFD were controlled to a great extent after successful development of
a formalin-inactivated vaccine produced in chick embryo fibroblasts. The
places where vaccination will be carried out are selected on the basis
of prevalence of KFDV activity in the previous years, including the villages
where monkey deaths were reported and those adjacent to the KFDV-affected
areas. The efficacy of the vaccine was satisfactory, exerting a highly
significant protective effect. Coverage of vaccine is fairly good. Almost
all individuals including children are being routinely vaccinated by local
government authorities. However, recent data on the incidence of KFD cases
from 5 districts of Karnataka state, namely Shimoga, Udupi, Mangalore,
Chickmangalore and Uttar Kannada suggest that the number of cases has increased
in the last 5 years. Total KFD cases: 85 in 1999, 130 in 2000, 435 in 2001,
625 in 2002, 920 in 2003, and 606 in 2004. In the month of January 2005
a total of 21 cases with 4 deaths were recorded. Increased KFD cases despite
routine vaccination suggests insufficient efficacy of the current vaccine
protocol. However, the exact cause of the increase in KFD cases needs further
investigation. The increasing trend of KFD cases in Karnataka state warrants
development of a new vaccine preparation that includes currently circulating
KFDV. Improper storage of vaccine and lack of maintenance of the
cold chain result in inactivation of the vaccine and could be another reason
for the emergence of KFD despite routine vaccination. Until now no quick
diagnostic kit has been available for early diagnosis of KFD. Most of the
cases are confirmed based on syndromic diagnosis, the HI, immunofluorescence,
and neutralization tests. Considering the requirement of safer and more
effective vaccines in general, there is clearly a need for developing an
alternative vaccine as well as a rapid diagnostic system for KFD,
but has also been shown to infect and cause disease in deer, cattle, goats,
grouse; vectors : Ixodes
ricinus),
meningitisand
acute
encephalitis
in humans
and headache,
followed by back and extremity pain, bradycardia, lymphadenitis,
conjunctivitis,
palantine injection, petechiae, and other hemorrhagic signs. Incubation
is 3-8 days.
and Ixodes cookei
(reservoir : small mammals and Capra
hircus)
(the majority)
(RSSE) after 4-20 days incubation : polio-like syndrome
in Bwamba county in Uganda. It causes mild febrile disease in certain areas
in Africa, especially in Nigeria.
and Bos taurus
and a mild febrile illness in humans
in South America, Sabethes cyaneus,
Aedes
africanus,
Aedes
luteocephalus,
the Aedes furcifer/Aedes
taylori
complex and Aedes simpsoni,
all of which breed in water-filled tree holes, in Central Africa; it occurs
in or near uncut forest or jungle. In more rural areas, these vectors --
and in eastern Africa, aedine mosquitoes, such as Aedes bromeliae
(formerly known as Aedes
simpsoni)
which breed in water-filled leaf axils of banana plants, plantains and
coco yams (Colocasia spp.) -- bite monkeys and humans and thus transfer
the virus from monkeys to the human population. Then ...
(anthropophilic mosquito which usually breeds prolifically in man-made
containers such as water-storage pots, discarded tin cans in and around
human villages and towns), bites humans and spreads the infection from
one human to another. In some previous outbreaks in the Sudan (such as
1940 and 1959) Aedes vittatusmosquitoes
there and starting an urban epidemic. Several such cases arrived in the
cities of Sao Paulo, Rio de Janeiro, Brasilia & Goiania in early 2000,
but fortunately there was no urban spread,
Aedes
taylori,
Aedes
luteocephalus.
Most importantly, the virus was isolated in male mosquitoes. Until recently,
the only known cycle had been that of Haddow in East Africa. The virus
circulate in the canopea between monkeys and Aedes africanus. These monkeys
infect Aedes bromeliae when they come to eat in banana plantations. This
cycle does not occur in West Africa. Vertical transmission is the main
method of maintenance of the virus through the dry season. "Reservoirs
of virus" are often mentioned in medical literature, monkeys having a short
viremia whereas mosquitoes remain infected throughout their life cycle.
In such a selvatic cycle, circulation can reach very high levels and no
child would be able to escape an infecting bite and yet no clinical cases
of yellow fever have been reported. The virulence--as it affects man--of
the yellow fever virus in its wild cycle is very low. In areas where the
virus can circulate in epidemic form, two types of circulation can be distinguished.
Intermediate yellow fever--a term coined to define epidemia which do not
correspond exactly to urban yellow fever. The cycle involves men and monkeys
through wild vectors as Aedes furcifer but also through Aedes aegypti
and the mortality rate is much lower than for urban epidemics. In urban
yellow fever, man is the only vertebrate host involved in the circulation
of the virus, the vector being generally Aedes aegypti. This vector
maintains a selective pressure, increasing the transmission of virus capable
of producing high viremia in man. In the selvatic cycles, 2 cycles can
be distinguished: one of maintenance which does not increase the quantity
of virus in circulation and one of amplification which does increase this
quantity. As we shall see, it develops into an epizootic form but also
in an epidemic form in man. When the decrease in yellow fevers across Africa
is considered, it appears that all major epidemics occur in West Africa
inspite of the presence of wild cycles of the yellow fever virus in Central
and East Africa. For the rare epidemics that have occurred there, the vector
has never been
Aedes aegypti. In a recent outbreak in Kenya, the
vector was Stegomyia
bromeliaeref.
The examination of part of the gene encoding for envelope protein showed
the presence of two geographical types corresponding to West-Africa and
Central East-Africa. Clinically speaking, yellow fever is an haemorrhagic
fever with hepatitis similar to other haemorrhagic fevers such as Rift
Valley fever. When, in 1987, an outbreak of haemorrhagic fever occurred
in southern Mauritania, for several days it was thought to be yellow fever.
Four days later, the diagnosis was corrected by isolating and identifying
the virus as that of Rift Valley fever
(RVFV)ref.
Old research showed that in the laboratory, Asian Ae. aegypti
mosquitoes were relatively incompetent vectors of YF. However,
the Amphur strain of Ae. aegypti from Thailand was not significantly
less competent than an East African or a Caribbean strainref,
and an "incompetent" strain did in fact vector a YF epidemic in 1987ref.
Note that Ae. aegypti has occasionally been imported into
Japanref.
,
chills, intense headache,
lumbago,
myalgia, nausea
and vomiting,
conjunctivitis,
dark urine, and bradycardia in relation to fever. After a 12-24 hour remission,
there is an "intoxication" or hepatorenal stage ("yellow stage")
(Councilman's
bodiesin
hepatocytes) that features reemergence of generalized symptoms including
increased temperature, increased nausea
and vomiting,
abdominal
pain,
jaundice,
and prostration. Complications of severe YF include jaundice
(hence the term "yellow"), dehydration, acute
renal failure,
delirium, and DIC
=> hemorrhagic symptoms in skin, mucosae, bowels (hematemesis
and melena), lungs, womb, spleen and kidneys. Terminal signs include
progressive tachycardia, intractable intractable
hiccup,
and shock : lethality 10-15% (in hyperacute forms within 2-3 days).
Atypical forms enclose myocarditis
and meningoencephalitis
=> coma
vigil / "typhoid status".
Lab findings include albuminuria, leukopenia,
abnormal liver function, increased prothrombin times. Treatment is supportive,
i.e, control of fever, nausea
and vomiting,
dehydration, and pain.
WHO has recommended that yellow fever be added to the list of child immunisation
vaccines in countries where the disease is endemic. A study
and
Eretmapoditeschrysogaster
with acute hepatitis
with rash in Central Africa;
sexual, parenteral (including blood transfusionref),
and vertical transmission have all been documentedref.
Thus, HIV-positive people have both a high rate of active GBV-C viraemia
(15-43%) and evidence of previous exposure to GBV-C (anti-E2 antibody in
31-55%)ref1,
ref2,
ref3,
ref4.
Inhibition of HIV-1
replication by GB virus C infection through increases in CCL-5
/ RANTES,
MIP-1, MIP-1ß, and SDF-1ref
and people coinfected with HIV and GB virus C (GBV-C) have lower mortality
than HIV-positive individuals without GBV-C infection,
GBV-C does not replicate in hepatocytes but replicates in vitro
in peripheral-blood mononuclear cellsref1,ref2,
ref3,
ref4,
including CD4+ T lymphocytesref,
CD8+ T lymphocytes, and B lymphocytes. After infection, viraemia
persists in 20-50% of exposed individualsref,
and clearance of GBV-C infection is in most cases associated with the development
of antibodies against the viral envelope glycoprotein E2ref1,
ref2.
: most infections are benign, but some develop chronic
hepatitis
G / syncytial giant-cell hepatitis after 2 weeks incubation. HGV has
been suggested as a cause of both fulminant and chronic hepatitisref1,
ref2.
However, when careful transfusion histories are obtained, it has been shown
that HGV infection occurs only after the onset of fulminant hepatitis and
after the patient has received blood productsref.
Where prospective studies of post-transfusion HGV infection have been carried
out, HGV can cause a mild hepatitis with ALT values usually < 200 U/l,
though there may often be no rise in liver enzymesref1,
ref2.
Most patients with persistent HGV infection do not have evidence of liver
disease, and coinfection with HCV does not appear to influence the course
of chronic HCV infectionref1,
ref2,
ref3,
ref4.
In addition, most studies suggest that HGV RNA is present in the sera of
approximately 1–2% of apparently healthy blood donorsref1,
ref2,
ref3.
Thus there is little evidence that HGV causes significant liver disease
and the clinical importance of the virus remains unclear.
?ref
(8.1% = 1.5-fold higher prevalence of infection in Hungaryref-15%
in Italyref)ref
(prevalence of HGV RNA at diagnosis = 2% in Japanref-3ref-6
(no difference between HCV+ and HCV-)ref-11%refin
Italy-7.1% in Turkeyref-9.26%
in Greeceref-10%
in UK (75% had undergone transfusion vs. 30% of HCV RNA-)ref--16.3%
in Germanyref-47%
in long term survivors of haematological malignancy in Birmingham (however,
over half the patients had undergone bone marrow transplantation)ref;
79% had past infection as seen with anti-HGV/E2 IgG in Italyref,
higher than that reported in healthy subjects, drug abusers and blood donorsref;
not involved in primary cutaneous B-cell lymphomas (CBCLs)ref).
,
Sus
scrofa
(the detection of HEV in 8 of 85 wild boar in 5 prefectures in Japan confirms
the suspicion that the outbreaks of HEV infection in Nagasaki and Tottori
prefectures in 2003 were initiated by the consumption of improperly cooked
wild boar meat), Ovis
aries,
Bos
taurus,Cervus
nippon nipponand
non-human primates are susceptible to infection). Zoonotic spread of HEV
is indicated by the fact that human and swine isolates of HEV are closely
similar in terms of nucleotide sequence, and experimental cross-species
transmission of swine HEV to a chimpanzee and of human HEV to swine have
been demonstrated
E / enterically transmitted non-A, non-B (ET-NANB) hepatitis. The period
during which an infected person can transmit the disease is unknown. Typical
signs and symptoms of hepatitis include jaundice,
anorexia, hepatomegaly,
abdominal
pain
and tenderness, nausea and
vomiting,
and fever,
although the disease may range in severity from mild to life-threatening.
Symptomatic HEV infection is most common in young adults aged 15-40 years.
Although HEV infection is frequent in children, it is mostly asymptomatic
or causes a very mild illness without jaundice that goes undiagnosed. It
has been claimed, however, that in endemic areas in India, HEV may be a
common cause of acute liver failure.
(0.5-4% in the general population) more often in economically deprived
communities, occurs more frequently in the 3rd trimester of pregnancy and
is associated with a CFR = 15-20% (eclampsia)
of viral genomes found in serum and faeces during the acute phase of the
disease or detection of antibodies during the convalescent stage (diagnostic
serologic tests are not available or licensed in many countries)
,
Sus
scrofa,
Gallus
gallus,
Felis
catus,
and other animals, the spike glycoprotein elicits an immune response from
the body, making it an attractive target for a vaccine
(72.7% (8 out of 11) vs 4.5% (1 out of 22) in control group test positive
for HCoV-NH by RT-PCR), the most common cause of acquired heart disease
in children in developed countriesref.
Ultimately, 2 specimens were identified in which the sequence of chemical
building blocks of the gene differed from that of known HCoV.
,
laryngotracheobronchitis) at all ages
.
The authors data are complex, and often there is evidence of co-infection
with other common respiratory tract viruses. Nonetheless, the authors come
to the reasonable conclusion that that HCoV-NL63 belongs to the group of
most frequently detected viruses in children under 3 years of age with
lower respiratory tract infections and that this virus is strongly associated
with croupref.
and epiglottitis
)
: endemic in many countries, including much of Africa, Asia, and South
America in all cloven-hoofed animals (Bos
taurus,
Ovis
aries,
Syncerus
caffer, alpacas, Erinaceidae,
Cervidae
); eradicated in the USA since 1929. Most of the FMD incidents have not
been associated with laboratory escapes but are related to the inadequate
inactivation of the virus with formalin, which has a tailing off in its
inactivation curve.
,
and later from mosquitoes and a mongoose in the same area; identified also
as the cause of an epizootic disease of swine in Panama.in
humans and encephalomyocarditis in Sus
scrofaand
certain nonhuman primates
,
headache,
myalgia, nausea and vomiting,
diarrhea,
self-limiting within 3-7 days. Complications : Gsell's myalgic meningitis,
myocarditis,
pericarditis,
acute
hepatitis
and orchitis.
=> congestive heart failure => sudden death
=>
congestive
heart failure => sudden death
associated with pulmonary
edema
and high case-fatality rates.
may persist for 4-5 days. A painless rash may also develop on the palms
and soles and sometimes on the buttocks, and there may be a loss of appetite,
especially if painful mouth ulcers make it difficult for the patient to
swallow.
or vesicular or petechial exanthema
,
headache,
myalgia, nausea and vomiting,
diarrhea,
self-limiting within 3-7 days. Complications : Gsell's myalgic meningitis,
myocarditis,
pericarditis,acute
hepatitis
and orchitis.
=>
congestive
heart failure or sudden cardiac death,
headache,
myalgia, nausea and vomiting,
diarrhea,
self-limiting within 3-7 days. Complications : Gsell's myalgic meningitis,
myocarditis,
pericarditis,
acute
hepatitis
and orchitis.
=> congestive heart failure => sudden death,
headache,
myalgia, nausea and vomiting,
diarrhea,
self-limiting within 3-7 days. Complications : Gsell's myalgic meningitis,
myocarditis,
pericarditis,
acute
hepatitis
and orchitis.
=> congestive heart failure => sudden death,
headache,
myalgia, nausea and vomiting,
diarrhea,
self-limiting within 3-7 days. Complications : Gsell's myalgic meningitis,
myocarditis,
pericarditis,
acute
hepatitis
and orchitis.
=> congestive heart failure => sudden death
or vesicular exanthema,
headache,
myalgia, nausea and vomiting,
diarrhea,
self-limiting within 3-7 days. Complications : Gsell's myalgic meningitis,
myocarditis,
pericarditis,
acute
hepatitis
and orchitis.
=> congestive heart failure => sudden death,
headache,
myalgia, nausea and vomiting,
diarrhea,
self-limiting within 3-7 days. Complications : Gsell's myalgic meningitis,myocarditis,
pericarditis,
acute
hepatitis
and orchitis.
=> congestive heart failure => sudden death
on cheeks => trunk => limbs.
=> congestive heart failure => sudden death
,
headache,
myalgia, nausea and vomiting,
diarrhea,
self-limiting within 3-7 days. Complications : Gsell's myalgic meningitis,
myocarditis,
pericarditis,
acute
hepatitis
and orchitis.
=> congestive heart failure => sudden death
=>congestive
heart failure => sudden death,
headache,
myalgia, nausea and vomiting,
diarrhea,
self-limiting within 3-7 days. Complications : Gsell's myalgic meningitis,
myocarditis,
pericarditis,
acute
hepatitis
and orchitis.
,
no fever
=> congestive heart failure => sudden infant death syndrome(generalized
newborn disease),
headache,
myalgia, nausea and vomiting,
diarrhea,
self-limiting within 3-7 days. Complications : Gsell's myalgic meningitis,
myocarditis,
pericarditis,
acute
hepatitis
and orchitis.
of which an epidemic occurred in Boston, Massachusetts
,
fever,
myalgia,
nausea and vomiting,
diarrhea,
self-limiting within 3-7 days. Complications : Gsell's myalgic meningitis,
myocarditis,
pericarditis,
acute
hepatitisand
orchitis.
=> congestive heart failure => sudden death
,
headache,
sore throats, nausea
and vomiting,
diarrhea
and constipation
self-limiting within 3-4 days. In some cases after 2-7 days
:
and attenuatedvaccines.
Even in areas that are now free of polio, long-term vaccination is needed
to protect against the occasional immunized individuals who can carry and
spread the disease. One man in Britain, for example, has excreted high
levels of poliovirus for 20 years; indeed, 14 carriers have been found
by chance since 1988.,
headache,
myalgia, nausea and vomiting,
diarrhea,
self-limiting within 3-7 days. Complications : Gsell's myalgic meningitis,
myocarditis,
pericarditis,
acute
hepatitis
and orchitis.
=> congestive heart failure => sudden death
).
mRNA translation is controlled by poly(rC)
binding protein 1 (PCBP1) and and PCBP-2
in persons with longer 157insMTTTVP isoform of TIM-1 (see hygiene
hypothesis).
from immune-mediated damage after 15÷50 days incubation :
and gastroenteric symptoms in adults.
.
expression
,
Aedes
funereus,Aedes
normanensis,
Aedes
procax,Culex
annulirostris
and Struthio camelus
are more sensitive than Gallus
gallus
(asymptomatic : blood samples taken at intervals are tested as "sentinels"
for the presence of EEEV or specific antibodies), other Aves
spp.,
or Equus
caballus
(adiness, listlessness, muscle spasms in the head and neck, tremors or
staggering, hind-limb weakness, erratic behavior, and a marked loss of
coordination. There is no effective treatment, and seizures resulting in
death usually occur in 48-72 hour in 90%. Equine epizootics occur in the
summer, but human infection is rare); vectors : Culiseta
melanura,
Aedes
vexans,
Aedes
albopictus,
Culex
taeniopus,
Culex
nigripalpus,
Coquillettidia
perturbans, and Ochlerotatus
sollicitans
,
headache, and nausea followed by drowsiness, convulsions, and coma.
Lethality : 30-80%. It is considered by CDC as a category B biological
weapon.
,
Aedes
aegypti,
Aedes
furcifer
and, where introduced, Aedes
albopictus
in Africa; in southeast Asia and Reunionref,
Aedes
albopictus
is a more competent vector than Aedes
aegypti).
Aedes
albopictus
appears to be a more competent laboratory
vector of chikungunya virus Aedes
aegyptiref
but as far as I know there has never been an actual isolation of the virus
from wild-caught specimens. Indeed, there seems to be no evidence that
Ae.
albopictus has actually been the vector of CHIK in any outbreaksref.
But it has long been suspected as a possible vector based on the culture
of the virus in cell lines and laboratory infections of female adult mosquitoes.
Several recent publications in the news media and scientific press, however,
say it is strongly suspected as a vector in Reunion. Other reports say
it is the vector. For example the paper by Martin Enserink in the journal
Scienceref
and the French Health Ministry both
declare it is the vector, but present no evidence. All I can add at this
stage is that a well-respected medical entomologist presently on an international
mission in Reunion believes the vector on the island is likely to be Ae.
albopictus, as does another renowned medical entomologist based in
a research laboratory in France who has worked on dengue. I might add that
the usual suspect vector, Aedes aegypti, is uncommon on Reunion,
and moreover the adults rarely bite peopleref.
Evidence for the role of Ae. albopictus in the transmission of chikungunya
virus remains rather unsatisfactory, but hopefully the vector on Reunion
will soon be identified, and if it proves to be Ae. albopictus,
this will show that this mosquito can -- at least in certain situations
-- transmit chikungunya virus. Non-human reservoir species
have not been identified unequivocally, and migrants and travellers are
blamed frequently for spread of infection,
headache,
bilateral arthralgias (70%) that may temporarily incapacitate
the patient, alimentary
features (nausea
and vomiting,
abdominal
pain,
possibly with jaundice),
sore throat, lymphadenitis,
maculopapular
exanthema
at defervescence, and malaise) lasting for 2 to 4 days with
recovery in 5 to 7 days.
Arthralgias remain a problem for weeks to several months after the acute
phase. Febrile convulsions may occur in young children. Compared with dengue
fever, chikungunya is distinguished by a briefer incubation period
and febrile episode, by persistent arthralgia in some cases, and by the
absence of fatalities. However, similarities between clinical appearances
of the 2 diseases probably account for misclassification and some underreporting
of chikungunya fever in areas with endemic dengue; therefore, laboratory
confirmation of reported cases is important.
and exanthema,
Anopheles
gambiae)
,
extremely pruritic morbilliform
maculopapular exanthema,
lymphadenitis,
and arthralgia,
Anopheles
amictus,
Aedes
aegypti,
Aedes
bancroftianus,
Aedes
camptorhynchus,
Aedes
eidsvoldensis,
Aedes
funereus,
Aedes
normanensis
( a floodwater mosquito, bites by day in the shade and at night),
Aedes
notoscriptus
(found only in urban areas where it breeds in artificial receptacles, bites
during the day in the shade and at night),
Aedes
procax,
Aedes
sagax,
Aedes
theobaldi,
Aedes
tremulus,
Aedes
vigilax(a
salt marsh mosquito, bites day and night),
Culex
annulirostris
(breeds in shallow water and bites after sundown and at night),
Culex
pipiens quinquefasciatus,
Culex
sitiens.
Humans exhibit significant viraemia and the virus can be maintained in
some epidemics in a human-mosquito-human transmission cycle.
of viral infection
,
maculopapular
exanthema
and painful bilateral acute
polyarthritis
may persist for weeks and occasionally months
,
bilateral arthralgia and maculopapular
exanthema.and
Equus
caballus
; vectors : Culex spp.,
Ochlerotatus
sollicitans,
Psorophora
confinnis
.)
and
maculopapular
exanthema.,
Rodentia,
snakes; terminal host : Equus
caballus
; vectors : Culex tarsalis,
Culex
pipiens quinquefasciatus,Aedesspp.,
Anopheles
spp.,
Culiseta
melanura
,
drowsiness, and convulsions. Lethality : 5-15%. It is considered
by CDC as a category B biological
weapon.,
isolated from Rodentia
in the Everglades National Park
,
splenomegaly,
mild fever,
...,
retronuchal, and posterior
cervical lymphadenitis
(differential diagnosis with measles) =4-10 days=> Forschheimer spots
: a fleeting exanthem consisting of discrete pink spots on the soft palate,
which may coalesce into a red blush and may extend over the fauces; sometimes
seen in rubella just prior to the onset of the skin rash (morbilliform
maculopapular exanthema
clearer than in measles and disappearing at pressure and spreading from
head to trunk and limbs), no mucosal involvement (differential diagnosis
with measles). Sequelae : arthralgia (50% of females) or arthritis (10%
of females) within 3 days since exanthema, postinfectious
encephalomyelitis (PIE),
thrombocytopenia
=> hemorrhages, mild heapatitis
=>,
pulmonary
valve stenosis
and pulmonary artery stenosis, septal defects) and ocular (congenital
cataract,
retinopathy,
microphthalmia,
congenital
glaucoma)
malformations, deafness, microcephaly, mental retardation, and generalized
growth retardation, sometimes associated with acute self-limited conditions
such as thrombocytopenic purpura, anemia, hepatitis, encephalitis, radiolucencies
of long bones, type
IA diabetes mellitus,
and autoimmune
hypothyroidism
(PRP) 10-20 years after acute infection. Lethal within some years.
and immunoglobulins.
particles, envelope proteins from HTLV-1
and HTLV-2
in VSV, influenzavirus
HA in Rous sarcoma virus particles, HTLV-1
envelope glycoprotein in HIV-1,
and
VSV G protein in both
murine retroviral and lentivirus vector particles. The low specificity
of the process governing glycoprotein incorporation into retroviral particles
is most likely responsible for the observation that retroviruses have been
found to incorporate certain cell-derived proteins in their envelope.
