Table of contents :
germ theory : the doctrine that infectious diseases are of microbic origin.
=> viroses
=> transmissible spongiform encephalopathies (TSEs)
=> mycoses
=> helminthiases,
and rarely meningitis
and endocarditis;
mixtures of every type occur, e.g., bacterial
and viral,
bacterial
and fungal,
and protozoan
and viral
caused 2.7 million (4.8%)
2.2 million (4.0%)
1.1 million (1.9%).,
...),
Ancylostoma
duodenale,
Strongyloides
stercoralis,
Sarcoptes
scabiei,
...))(vertical
transmission)
of infected blood or derivatives (transfusion-associated transmission (TAT))
(for parasites with a hematic stage)
of infected organs
joint infections caused by injectable steroidsref;
Pseudomonas
spp.
and Serratia spp.
infections, resulting in meningitis from epidural injections (CDC, unpublished
data, 2002; Contra Costa Health Services, unpublished data, 2002); Burkholderia
cepacia
blood stream infections from intravenous flush (CDC, unpublished data,
2004), and Pseudomonas
fluorescens
blood stream infections from intravenous flush. Regulatory oversight of
compounding pharmacies varies among states. However, compounding pharmacies
are subject to inspection by pharmacy boards, FDA, and accreditation organizations.
The American Society of Health-System Pharmacists and the U.S. Pharmacopeia
have developed guidance and standards that address quality assurance and
sterile preparation of compounded products (American Society of Health-System
Pharmacists. ASHP technical assistance bulletin on quality assurance for
pharmacy-prepared sterile products. Am J Hosp Pharm 1993; 50:2286-98. U.S.
Pharmacopeial Convention, Inc. U.S. pharmacopeia 28 [Chapter 797]. Pharmaceutical
compounding: sterile preparations. Rockville, MD: U.S. Pharmacopeial Convention,
Inc.; 2004:2461-77). In addition, in May 2004, the Pharmacy Compounding
Accreditation Board (PCAB) established a task force to set standards for
a voluntary accreditation board for compounding pharmaciesref.
Companies that manufacture products intended for injection should follow
FDA regulations for ensuring the sterility of these productsref.
Treatment for potential patients should include targeted antimicrobial
therapy and consideration of removing their cathetersref.
,
endotracheal
intubation,
endovenous
catetherism,
urinary
catheterism,
cardiovascular
prosthesis,
surgical
sutures.)ref
(from foods preserved in olive-oil) : incubation = 8-36 days; duration
= days to 1 year
(from pastries, salads, remnants, protein-rich foods) : 1-8 hours (usually
< 6-hour) incubation period; mostly nausea and vomiting, diarrhea, abdominal
cramping; lasting for 24-48 hours
(from meat (expecially chicken)) : incubation period 8-22 (12-18) hours
(average 12), more diarrhea; lasting for 24 hours
(from starch-rich foods (e.g. rice, pasta), cereals, sauce, spices, Chinese
restaurants) : incubation period = 30'-5 hours; duration = 6-24 hours,
and more prolonged symptoms are more likely due to the in situ replication
of enteric pathogens
(up to 72 hours)
(from unpasteurized milk and derivatives, salad) : incubation = 1-7 days;
duration = 1-3 days
(from chicken, eggs, meat, fish, milk and derivatives) : incubation = 6-72
hours; duration = 2-3 days
(from animal bowels, field, milk, meat, shellfish, cheese) : incubation
= 1 day-3 weeks
: in 1996 and 1998, there were 2 episodes involving rabid cows that occurred
in Massachusettsref.
Milk from rabid cows can contain rabies virus, and transmission via unpasteurized
milk is theoretically possible. Temperatures reached during pasteurization
kill the virus. 80 persons consumed unpasteurized milk that was collected
from the 2 cows, and 9 more had contact with saliva from the cows. All
89 persons received postexposure rabies prophylaxis, and no human cases
of rabies eventuated. A similar report in Oklahoma of possible rabies exposure
associated with the consumption of raw milk or cream from a rabid cow was
circulated in 2006,
a zoonotic arbovirus infection usually transmitted to humans by the bite
of an Ixodes persulcatus or Ixodes ricinus tick, is endemic
to Central Europe, Eastern Europe, and Russiaref.
However, the virus can be found in the milk of cows and goats with tickborne
encephalitis and was reported to be transmissible to humans by the consumption
of unpasteurized milkref.
A case-control study failed to confirm oral transmissionref.
(including multidrug-resistant strains)
and HAV)
: theoretically any infectious organism can be transmitted
might depend on several factorsref,
including :
ref1,
ref2,
ref3ref1,
ref2ref1,
ref2,
ref3,
ref4refref1,
ref2
were originally described during outbreaks among American military personnel
during the 1950s. These agents accounted for about 72% of all respiratory
disease and 10% of hospitalization among recruits in 1958. Military outbreaks
tend to involve adenovirus types 4 or 7. Adenoviruses were implicated in
53% of respiratory disease among military trainees during 1996 to 1998.
2 recruits died of adenovirus infection in Illinois in 2000, the 1st fatalities
among military personnel since 1972. A live oral vaccine was released in
1971 for routine use in the military : recent discontinuance of vaccination
has been followed by large outbreaks of acute respiratory diseaseref1,
ref2.
Notable outbreaks:
was 1st isolated from American military personnel in 1944. At the time,
the organism was estimated to account for 68% of "atypical pneumonias"
among recruits. As many as 57% of recruits had evidence of acute infection,
and up to 56% of pneumonia among recruits during the 1960's to 1990's was
ascribed to this organism. Notable outbreaks:
was detected in 21 mineral waters of 11 different brands of European mineral
waters by RT-PCR. All isolated NLV gg I strains have a similarity of 70
to 87% with the common Desert Shield virus (UO4469), and all isolated NLV
gg II strains have a similarity of 89 to 93% with the Camberwell virus
(U46500). The presence of NLV sequences could not be correlated either
with bottle characteristics or with chemical properties like mineralization,
pH, or the presence of carbonic acidref.
In a following study NLV sequences belonging entirely to genogroup II were
detected in 33% of samples without gases analyzed in the range of 10 to
100 genomic equivalents per liter. After 6 months, all samples remained
positive; after 12 months, 90% samples were still positive for NLV sequences,
suggesting that an envelope of proteins surrounds the virus protecting
its RNA and possibly still allowing infectiveness (not tested anyway)ref.
Human faeces are sporadically contaminating the water either at the source
or some time during the bottling procedure. Unpublished evidence suggests
that low levels of the virus in mineral water may give some elderly people
gastroenteritis.
among among injecting drug users (IDUs) in the UK who had 1st injected
in the last 3 years was 18%, double the prevalence among this group in
2000 (9%) and earlier years. Between Apr and Dec 2003, 18 cases of methicillin-resistant
Staphylococcus
aureus
(MRSA) blood infection were identified among IDUs. Laboratory tests of
the MRSA isolates show they are different from those associated with healthcare.
Severe group A Streptococcus
spp. (GAS)
reports among IDUs have increased, from less than 10 per annum in the early
to mid-1990s to 160 in 2003. An outbreak of tetanus,
which started with 11 cases reported in 2003, has continued into 2004.
While during 2003 there were also 14 reports of suspected cases of wound
botulismamong
IDUs, 7 of which were confirmed by laboratory tests. Although an effective
needle exchange program to minimize blood-borne infection transfer may
minimize HBV
and HCV,
bacterial infections due to streptococci and staphylococci as well as toxemias
from clostridrial infection (tetanus, botulism) will likely persist, as
they are related to the contaminated drug itself or are already present
on the skin of the userref,
which killed an estimated 30,000 people,
which affected 50 million people and killed approximately 25,000,
with up to 50,000 estimated cases and up to 15,000 estimated deaths,
which affected up to 300,000 people and killed about 5,000,
which killed 774 of the 8102 people infected
- for which an effective vaccine exists - is estimated to affect 200,000
peopleref
: vector of Toxoplasma
gondii
: vector of Dientamoeba
fragilis
,
Borrelia
hispanica
,
Ehrlichia
chaffeensis,
Ehrlichia
ewingii,
Francisella
tularensis;
found on the atlantic coast of USA from New York southwards to Virginia,
Georgia, New England and Florida and extending westwards into Texas
and Oklahoma (also causing tick
paralysis)
.
An “engorgement factor" termed voraxin (a cocktail of 2 peptides
that are upregulated in the testis and vas deferens of fed, but not unfed,
males : they have no effect on female feeding if given alone) transferred
from male ticks to females during copulation not only stimulates the females
to gorge on food, but also stimulates the development of the ovary and
the degeneration of salivary glands, preparing females for the reproductive
tasks ahead. The feeding cycle of adult female ticks is divided into preparatory,
slow and rapid feeding phases. At the transition from slow to rapid feeding,
females reach a 'critical weight' (CW; approx. 10x the unfed weight) that
is characterized by several behavioural and physiological changes. 5 of
these changes were used as criteria to establish a more precise estimate
of CW than we have to date. The CW as defined by re-attachment to the host
was 9x the unfed weight, while for haemolymph ecdysteroid titre, salivary
gland degeneration, ovary weight, oocyte length and oocyte vitellin content
the CW was 10x, 10x, 12x, 12x and 13x, respectively. CW thus varies depending
on the parameter measured. Although previous studies have established the
influence of ecdysteroids on salivary gland degeneration and vitellogenesis,
they also have a role in inhibiting re-attachment to the hostref.
Virgin female will not feed beyond a CW of around 10 times their unfed
body mass, but mated ticks will. There was already evidence that components
of seminal fluid can have important behavioral and physiologic consequences
for females, e.g. in D. melanogaster seminal fluid protein genes
expressed only in males affect female receptivity, ovulation, oogenesis,
sperm storage, sperm competition and mating plug formationref.
It is interesting that sex proteins also occur in noninsect species like
ticks because this suggests that these male factors could be quite ubiquitous.
In the case of the tick, it appears that these sex peptides are acting
in the reproductive interests of both sexes. It's a kind of switch effect
to tell females that they've been properly mated : iIt's only worth starting
to produce eggs and develop your ovaries once you have been mated. If an
effective vaccine can be derived from voraxin, the anticipated results
from reduced feeding would include less salivation, hence reduced pathogen
transmission to the host and a reduction in oocyte development. When normal
mated females were put on a rabbit immunized against voraxin, 74% showed
little interest in feeding, but all mated ticks put on a control, nonimmunized
rabbit engorged normally. So, a vaccine that blocks the action of voraxin
should reduce feeding, argued Kaufman, and hence transmission of tick-borne
pathogens such as the bacterium Ehrlichia ruminantium, which causes
a Rickettsia-like infection in African cattle : it is argued whether voraxin-based
vaccine would achieve better control of ticks than existing vaccines based
on antigens from the southern cattle tick Boophilus microplus
,
Colorado
tick fever virus,
and Francisella tularensis
to humans and for causing tick
paralysis
in Rocky Mountain and western areas of the USA and Canada. Its hosts include
Cervidae,
elk, antelope, grizzly bear, porcupine,
Cynomys
parvidens , and various
Oryctolagus
spp..
,
Francisella
tularensis,
Ehrlichia
chaffeensis
and Anaplasma
phagocytophilum
(also causing tick paralysis)
,
Borrelia
burgdorferi
,
Anaplasma
phagocytophilum
,
Borrelia
burgdorferi,
Rickettsia
helvetica
,
tick-borne
encephalitis virus (TBEV),
Babesia
divergens,
Borrelia
burgdorferi,
and Colorado tick
fever virus
,
Anaplasma
phagocytophilum
,
Rickettsia
rickettsii,
Rickettsia
conorii,
Borrelia
burgdorferi,
Borrelia
theileri,
Ehrlichia
chaffeensis
and Gnathostoma
spinigerum
,
Treponema
carateum
,
Salmonella
typhi,
minor
or non-typhi Salmonella spp.,
Vibrio
cholerae,
polioviruses
vectors of Mansonella streptocerca
,
o'nyong-nyong
virus
,
Western
equine encephalomyelitis virus (WEEV)
and Vesicular
stomatitis virus serotype Chandipura,
yellow
fever virus (YFV),
Ross
River virus,
Barmah
Forest virus,
Murray Valley encephalitis virus,
Chikungunya
virus.
It does not breed in ricefields, but favour man-made and natural container
habitats. The vectors of dengue in Africa include the presumed ancestral
subspecies of the cosmotropical
Ae. aegypti, which breeds predominantly
in phytotelmata (water collections in plants) in rural and sylvatic
zones, as well as the subspecies described in the editorial comments as
breeding in artificial containers (Ae. aegypti formosus and
Ae.
aegypti aegypti). It is generally agreed that
Aedes aegypti
originated in Africa and spread to much of the tropical world. It is true
that a black (dark) form of adults called
Ae. aegypti formosus breeds
in natural container habitats (e.g. tree-holes) in mainly forested areas
away from human habitations in parts of sub-Saharan Africa. It rarely
bites humans. This form is essentially confined to Africa although it has
been transported to a few islands. However, it is the browner and
lighter form Ae. aegypti sensu stricto (Ae. aegypti aegypti)
that is the main vector of dengue, whether in Africa or in other parts
of the world. This is the species that colonises man-made container habitats
such as water-storage pots and consequently has close contact with humans
and is highly anthropophagic. However, the issue is not that simple, as
these 2 forms may very occasionally interbreed and give rise to adults
showing differing degrees of paleness. Moreover, in East Africa there is
evidence that the dark form (ssp. formosus) has become peridomestic
and breeds in man-made containers and footholds cut in coconut palms. But
basically when Ae. aegypti is cited as a dengue vector it refers
to the paler form. For example, virtually all types of water receptacles
such as water barrels, discarded tin cans, broken bottles, large water
tanks and very commonly water-storage pots -- whether they be inside
or outside houses -- are colonised by Ae. aegypti larvae. Larvae
are also found in cemetery urns and flower vases, and less commonly in
wells, but that is mainly where there are few water-storage pots. Larvae
are not found in waters polluted with urine or feces, such as cess pits
and septic tanks. They are often said to be found in clean waters, but
usually such waters contain some amount of organic matter. For instance,
in Kenya, water-storage pots where people wash their hands after eating
were the most productive breeding sites, as larval food was plentiful in
such pots. Whether or not Ae. aegypti larvae are present in stagnant
waters depends on what is meant by stagnant! If it means "still,
as opposed to flowing, water" -- then yes, this mosquito does breed in
such waters. But stagnant can also mean foul or polluted waters. It then
further depends on the definition of foul and polluted waters, because
Ae.
aegypti can be found in waters containing considerable detritus or
organic materials such as human food (see above), but not in waters contaminated
with urine, feces, or decomposing animal material. Only very rarely have
Ae.
aegypti larvae been found in ground collections of water, but in some
areas (mainly rural), larvae are commonly found in tree-holes and more
occasionally in water-filled leaf axils of plants such as Colocasia
(coco-yams). Larvae have occasionally been found in atypical habitats,
such as non-chlorinated (and usually abandoned) swimming pools, but such
larval habitats will rarely produce sufficient numbers of adults
to be of any importance in dengue situations. There are several incidences
of Ae. aegypti being eradicated from areas only to reappear, sometimes
after many years. For example, in the 1970s this mosquito was eradicated
from a number of South American countries, but by the mid 1990s Ae.
aegypti had reinvaded many of them. With regard to Australia, populations
of Ae. aegypti in Queensland were greatly reduced in the 1970s,
but after an absence of 26 years, dengue was again reported from Queensland
in 1981/82. Isolated also in New Zealand but it occurs in many areas of
the world where there is no YFV, for example the Indian subcontinent. Larval
habitats of this species comprise almost any man-made container habitats,
including water-storage pots, discarded utensils such as cans and bottles,
flower pots, wells, and gutters to buildings -- although in some situations
larvae occur in natural container habitats such as water-filled rot holes
in trees and rock pools. All these habitats are characterised by clean
water or water with a moderate amount of organic material such as leaves
or residues of human food (upon which the larvae feed) that is so-called
dirty water, but larvae never occur in cess pits, septic tanks or any other
waters contaminated with urine, feces or rotting carcasses. So it would
be very unusual if in this instance in Kolkata that Ae. aegypti
were to be found in pit latrines; it is much more likely that larvae of
Culex
quinquefasciatus (vector of bancroftian filariasis, Wuchereria bancrofti)
were present in such organically polluted waters..
A Breteau index of 35-49 is often taken as the critical threshold
for dengue transmission, but there are several instances where the occurrence
of dengue/DHF has no relationship with either the Breteau or House indicesref.
In fact there are many important variables, such as human population
density, distances between houses, single storey versus multi-storey dwellings,
and whether positive water pots contain just a few or many Aedes aegypti
larvae, that can be epidemiologically important in disease transmission.
In summary the relationship between larval or pupal density figures and
epidemic risk is at best dubious. The value of such indices has been criticised
because outbreaks of diseases like dengue depend on many other factors
such as the actual numbers of larvae per container, the percentage that
survive to complete development and give rise to adults, and
the population density of humans. Eradication campaigns in the 1940s and
1960s eliminated Ae. aegypti from many Central and South American
countries, including Paraguay, but after such programs ceased in
the early 1970s, Ae. aegypti reappeared in most of those countries.
Another dengue vector, Ae. aegypti, originally from Asia, was found
in the 1980s and 1990s in some Latin American countries. It was not
been found in Paraguay, although it has been recorded in Brazil ( in 1986)
and Argentina (in 1998). Ammonia as an attractive component of host odourref.
In 1973 WHO tried to simplify matters by correlating these various
indices; they introduced density figures (1-9) which corresponded
to ranges of the above 3 larval indices. For example, a density figure
of 5, representing a House index of 29-37, a Container index of 15-20 and
a Breteau index of 35-49, was in the case of yellow fever taken to indicate
a threat of urban transmission. However, these density figures have rarely
been used and the most widely used index is the Breteau Index. But
in a recent study in Brazil while both the House and Breteau indices were
often zero or close to 0, the container index was sometimes as high as
11%. The authors concluded that in their study the Container index was
the best indicator of Ae. aegypti larval population sizeref.
There are clearly difficulties in interpreting the various larval indices.
Another index is the egg index, which detects egg laying. This can
be monitored by using cheap and simple ovitraps that commonly consist of
a strip of absorbent material, e.g. hardboard or velour paper, placed in
a tin can or jar containing water. Female Ae. aegypti deposit their
eggs on the wet strip. The percentage of such traps with eggs of Ae.
aegypti can provide some measure of the relative population size of
the vector.
,
Chikungunya
virus,
Dirofilaria
spp.,
dengue
virus
(potential vector, having spread since the 1970s to the USA and Canada,
several countries in Latin America and Europe and elsewhere, but not to
Yemen),
EEEV,
Chikungunya
virus,
Rift
Valley fever virus,West
Nile virus (WNV)ref1,
ref2,
ref3,
and more yellow fever
virusto
animals and humansref
. The susceptibilty varies genetically, and it is a relatively poor vector
of epidemic strains of arboviruses, including dengue, but it may
be more important in transmitting "endemic" strains. It does not breed
in ricefields, but favour man-made and natural forest container habitats
(e.g. water-storage pots, tree-holes, and tires). Aedes albopictus
larvae are also found in water-storage pots and discarded tin cans, etc.,
but also in rain water that accumulates in tires, either abandoned ones
or those being used for retreading (remoulding). But this species is more
commonly found in water-filled tree-holes, cut bamboo stumps and leaf axils
than Ae. aegypti. Basically Ae. albopictus is less
well-adapted to city life than Ae. aegypti. It lays eggs in cut
bamboo, rock pools and tree holes, but in urban situations most oviposition
is in domestic water containers, discarded utensils such as bottles, jars
and tin cans, and vehicle tires. Control is normally directed at removing
peridomestic larval habitats, for which community participation is usually
necessary. In epidemic situations, or threats of epidemics, insecticidal
spraying may be used to kill mainly adult mosquitoes, including virus-infected
ones. It was 1st found breeding in the USA in 1985 in Houston, Texas. Since
then, it has gradually spread further north, to northern New Jersey along
the Atlantic coast, and to Illinois. By 2003, it had spread to 28 US States.
But this is not the first time it has been reported from California. Larvae
were found in 1971 in tires off-loaded in Oakland from a ship from Viet
Namref.
It would be interesting to learn exactly how this mosquito arrived in California
aboard a pleasure boat towed from the south east. It was incriminated as
a vector of dengue in Hawaii in 2001. In 2000, it was found infected with
West Nile virus in Pennsylvania. In much of the USA, however, it seems
more likely that it could be a bridge vector of indigenous viruses like
La
Crosse virus,
Venezuelan
equine encephalitis virus (VEEV)
and EEEV
,
Barmah
Forest virus,
Ross
River virus,
and Kokobera virus
(and Murray
Valley encephalitis virus),
none of which has been reported from New Zealand
and Simbu virus,
Murray
Valley encephalitis virus,
Barmah
Forest virus
and yellow fever virus
(transovarial transmission),
Barmah
Forest virus,
Murray
Valley encephalitis virus
,
Ross
River virus,
Murray
Valley encephalitis virus,
Wuchereria
bancrofti
(only on various Polynesian islands) and minor vectors of Ross
River virus
and Murray
Valley encephalitis virus.
Isolated also in certain Pacific Islands and in New Zealand,
Barmah
Forest virus
,
Murray
Valley encephalitis virus
,
Murray
Valley encephalitis virus,
Ross
River virus,
Murray
Valley encephalitis virus
epidemic in the Arabian Peninsula
,
Ross
River virus,
Murray
Valley encephalitis virus
,
Bunyamwera
virus,
Uganda
S virus,
Ross
River virus,
Kunjin
virus,
Barmah
Forest virus
,
Kunjin
virus
,
Murray
Valley encephalitis virus,
Wuchereria
bancrofti
and Banna virus
and West Nile virus (WNV),
Saint
Louis encephalitis virus
,
Saint
Louis encephalitis virus
between themref,
Western
equine encephalomyelitis virus (WEEV),
Murray
Valley encephalitis virus,
Kunjin
virus,
Ross
River virus
and Japanese encephalitis
virus
(isolates have been obtained from this species in Malaysiaref
and Northern Taiwanref.
Malaysian and Australian Cx. sitiens strains were able to transmit
the virus in laboratory-based vector competence experimentsref1,ref2.
Furthermore, high rates of pig feeding have been reported from Cx. sitiens
in Malaysiaref.
Finally, Cx. sitiens is a member of the Cx. sitiens subgroup,
which includes Culex annulirostris, the primary vector of JEV in
Australiaref),
Saint
Louis encephalitis virus,
Western
equine encephalomyelitis virus (WEEV),
West
Nile virus (WNV),
living in freshwater collections, extremely common in rice fields throughout
much of Asia
and Banna virus,
Everglades
virus (EVEV)
and EEEV
in New York State. The larval habitats of this species consist primarily
of ground pools, roadside ditches, and pools at the edge of marshy areas
,
Okola
virus,
Rift
Valley fever virus,
Simbu
virus,
Spondweni
virus
,
Rift
Valley fever virus,
Murray
Valley encephalitis virus,
Kunjin
virus
and Vesicular
stomatitis virusref
and Toscana virus,
Leishmania
major,
Leishmania
tropica,
Toscana
virus,
Leishmania
infantum,
Leishmania
major,
Leishmania
tropica
,
Trypanosoma
conorhini in rodents (Rattus).
,
Yersinia
pestis,
Trypanosoma
conorhini in rodents (Rattus).
,
Rickettsia
felis
,
Bartonella
henselaeref
,
Yersinia
pestis
,
Aspergillus
spp.
and Penicillium spp..
Information about the carriage of pathogenic fungi by cockroaches in hospital
environment is scanty. The results suggest that cockroaches can play a
role in dissemination of fungi, which they can carry on their external
surfaceref.
Although females have a fully formed reproductive tract through which they lay eggs, they don't use it for copulation. Instead, a male penetrates a female's abdomen with a sharp, intromittent organ called a paramere, and injects his sperm directly into her body cavity, from where they migrate to her ovaries. So-called extragenital traumatic insemination visibly scars females, and a high mating frequency reduces a female's lifespan. But females have responded with a counteradaptation of their own, a structure called a spermalege situated on a female's right flank, where she is most frequently penetrated. It consists of a groove in the outer cuticle that guides the male's paramere through the cuticle into an underlying membrane-bound sac rich in haemocytes, suggesting a role for the spermalege in the control of pathogens introduced during insemination and repeated physical trauma.
has been isolated from sylvatic animals as far north as the state of Maryland
in the US, but no human infection has been reported thereref.
There are numerous sites in Texas where the bugs have been collected, and
a genetic algorithm for rule-set prediction-generated ecologic niche model
predicts a large area of infestation. Unlike the case in most of South
and Central America, triatomid bugs have actually been collected from areas
near suburban housesref.
There are some 120 species of triatomine bugs belonging to 17 genera, the
most widely known being Triatoma. 106 species only occur in the
New World, 7 species (all in the genus Triatoma ) are found in Asia,
and 6 species, belonging to the genus Linshcosteus, occur in India,
mainly in the south.
- Triatoma rubrofasciata (a.k.a. Triatoma rubrofasciatus, large kissing bug) is common in Asia (urban and rural), but it is also found in Africa, the New World, including the USA, and, among the many Asian countries, it occurs in India. It is the most cosmopolitan triatomine bug. It occasionally feeds on humans, a bite that often leads to significant local swelling and sometimes severe systemic reactions. This bug is also responsible for transmission of Trypanosoma conorhini in rodents (Rattus).
,
Rickettsia
prowazekii
and Borrelia recurrentis
,
Metorchis
conjunctus
,
Schistosoma
intercalatum Zaire
in Japan and the second most important in China, as well as a carrier of
the flukes Opisthorchis
felineus
and Echinochasmus perfoliatus)
,
Clonorchis
sinensis,
Opisthorchis
felineus,
Opistorchis
viverrini,
Anisakidae,
Gnathostoma
spinigerum,
Capillaria
philippinensis,
Chlamydophila
psittaci
,
Clostridium
botulinum serotype E,
Burkholderia
pseudomallei,
Crimean-Congo
hemorrhagic fever virus,
Newcastle
disease virus (NDV) / avian paramyxovirus 1,
Influenzavirus
A H1,
Influenzavirus
A H2,
Influenzavirus
A H3,
Influenzavirus
A H4,
Influenzavirus
A H5,
Influenzavirus
A H6,
Influenzavirus
A H7,
Influenzavirus
A H8,
Influenzavirus
A H9,
Influenzavirus
A H10,
Influenzavirus
A H11,
Influenzavirus
A H12,
Influenzavirus
A H13,
Influenzavirus
A H14,
Influenzavirus
A H15
,
Murray
Valley encephalitis virus,
West
Nile virus (WNV),
Ilheus
virus (ILHV),
Kyasanur
forest disease virus (KFDV),
EEEV,
Western
equine encephalomyelitis virus (WEEV)
.
,
Rickettsia
typhi
,
Leptospira
interrogans serovar icterohaemorrhagiae,
foot-and-mouth
disease virus (FMDV)
,
Thottapalayam
virus
,
Leishmania
tropica
,
lymphocytic
choriomeningitis virus (LCMV)
,
Leishmania
braziliensis
,
Puumala
virus (PUUV)
,
Yersinia
pestis
,
Hymenolepis
nana,
Trypanosoma
cruzi,
Rickettsia
akari,
ectromelia
virus (EV),
rabies
virus,
mouse
mammary tumor virus (MMTV) / Bittner virus,
lymphocytic
choriomeningitis virus (LCMV)
,
Hymenolepis
nana,Trichinella
spiralis,
Capillaria
hepatica,
Trypanosoma
cruzi,
Leishmania
braziliensis,
Balantidium
coli,
Streptobacillus
moniliformis,
Rickettsia
typhi,
Spirillum
minus,
rabies
virus
,Leptospira
interrogans serovar icterohaemorrhagiae,
Seoul
virus
,
Yersinia
pestis,
Seoul
virus,
SARS
coronavirus
),
ratpoxref1,
ref2,
and, extremely rarely, rabies virus
,
Laguna
Negra virus
,
Cano
Delgadito virus,
Leishmania
mexicana mexicana
,
Leishmania
braziliensis
,
Leishmania
braziliensis
,
New
York hantavirus
,
Sin
Nombre virus
,
Rickettsia
prowazekii,
Francisella
tularensis
,
monkeypox
virus,
Francisella
tularensis
,Taenia
serialis,
Angiostrongylus
costaricensis,
Leishmania
infantum,
Babesia
microti,
Streptobacillus
moniliformis,
Rickettsia
conorii,
Burkholderia
pseudomallei,
Yersinia
pseudotuberculosis,
Pichinde
virus,
Sabia
virus,
California
encephalitis virus,
rabies
virus,
Venezuelan
equine encephalitis virus (VEEV),
Western
equine encephalomyelitis virus (WEEV),
cowpox
virus,
Lagos
bat virus
,
Nipah
virus
.
The result that between 6-19% of the Daubenton's bats tested positive for
the EBLV-2 antibodies should be interpreted with caution; the range is
so great because blood samples of a number of bats were pooled in order
to provide a large enough sample to be tested.
,
Rio
Bravo virus,
Melaka virus
Bats comprise 20% of the diversity of mammalian species, so it should not be surprising that they are the zoonotic host for a number of infections. Expert opinion is that they are not over-represented as hosts for infectionsref. Why infections endemic in bats should be so pathogenic in humans is less clear, but may relate to the (currently poorly understood) bat immune system: bats, lacking bone marrow in their hollow bones, may have different antiviral responses, possibly including viral inhibitors. What are the implications for humans and bats in Europe? Horseshoe bats are widely distributed from Australia to Europe, but the species cited in the Chinese study are not indigenous to Europeref. Bat migration and trade in bats for traditional medicines have the potential to introduce new infections into European bat species. There are also risks from the spillover effect: intermediary species may be imported having already acquired infection from bats, or could acquire infections already endemic in European bats (Muller T, Cox J, Peter W, Schafer R, Johnson N, McElhinney LM et al. Spill-over of European bat lyssavirus type 1 into a stone marten (Martes foina) in Germany. J Vet Med B Infect Dis Vet Public Health 2004;51:49-54). Finally, global travel and migration mean that new human infections arising anywhere in the world could potentially become a problem in Europe. Hollow bones and lack of bone marrow is a flight adaptation common to birds as well as bats. It is likely just that, a flight adaptation and an immune status alteration. Likewise, disease may be passed between species by housing them in close proximity and in overcrowded conditions, such as those occurring in many markets in China. Although there are clearly some diseases associated with bats, possibly transferred to humans (such as rabies), it is just as likely that viruses may be obtained from eating unhealthy animals or under unsanitary conditions, such as eating fruit regurgitated by any animal. Incidentally, 5 of the 7 recognized groups of lyssaviruses are bat viruses. The 2 exceptions are classical carnivore rabies virus and Mokola virus (vector unknown).
.
Civets, a fruit-eating relative of mongooses, have a strong taste and are
a seasonal delicacy in Guangdong, where their consumption in November and
December is widely believed to help people keep warm throughout the winter.
,
(19.4%), Taenia
hydatigena
(7.4%), Taenia solium,
Taenia
serialis,
Taenia
pisiformis
(11.8%), Taenia multiceps,
Taenia
taeniaeformis,
Toxocara
canis
(1.2%), Ancylostoma
braziliense,
Ancylostoma
caninum,
Uncinaria
stenocephala,
Trichuris
vulpis,
Strongyloides
stercoralis,
Babesia
microti,
Anaplasma
phagocytophilum,
Ehrlichia
canis
(canine granulocytic ehrlichiosis (CGE)), Ehrlichia
chaffeensis,
Dirofilaria
immitis,
Dirofilaria
repens,
Trypanosoma
rangeli,
Trypanosoma
cruzi,
Leishmania
donovani chagasi,
Leishmania
infantum,
Leishmania
braziliensis,
Leishmania
peruviana,
Isospora
belli,
Brucella
melitensis biovar Canis,
Rickettsia
conorii,
Yersinia
pestis,
Leptospira
interrogans serovar canicola,
pseudorabies
virus (PrV) / Aujeszky's disease virus (ADV) / suid herpesvirus 1,
cowpox
virus,
canine
distemper virus (CDV),
Nipah
virus,
SARS
coronavirus,
Capnocytophaga
cynodegmi,
Pasteurella
dagmatis,
Pasteurella
multocida,
rabies
virus
(9.4%), Enterocytozoon
bienuesi
,
Leishmania
infantum.
(can become infected through flea bite, but most acquire plague through
ingesting plague-infected rodents), Leptospira
interrogans,
pseudorabies
virus (PrV) / Aujeszky's disease virus (ADV) / suid herpesvirus 1,
cowpox
virus,
Nipah
virus,
Pasteurella
dagmatis,
Pasteurella
multocida,
Afipia
felis,
Sporothrix
schenckii
(33-55.2%; a higher percentage is noted in the groups of indoor kept cats
of 1-6 month (27.1%) than that of outdoor kept cats of 1-6 month (17.9%),
7 month-1 year (18.5%) and 4-5 year (14.3%)), Dipylidium
caninum
(20.7%), Campylobacterjejuni
(0.8-1%), Salmonellaenterica
serotype Typhimurium
(0.8%), Cryptosporidium
parvum
(3.8-5.4%), Giardia intestinalis
(2.4-7.3%), Toxoplasma
gondii,
Ancylostoma
braziliense,
Ancylostoma
caninum,
Trypanosoma
rangeli,
Trypanosoma
cruzi,
Leishmania
donovani chagasi,
Helicobacter
felis.
At least 1 zoonotic agent is detected in 13.1-40.7% of samples..
.
,
Mycobacterium
bovis
,
Influenzavirus
A
.
,
Influenzavirus
A H7,
Influenzavirus
B
,
Trichinella
britovi
,
Yersinia
enterocolitica,
Yersinia
pseudotuberculosis
,
Taenia
pisiformis,
Taenia
taeniaeformis,
Otobius
lagophilus,
Yersinia
pestis,
Francisella
tularensis,
monkeypox
virus,
Mycobacterium
avium subsp. paratuberculosis,
Pasteurella
multocida
(rhinitis, otitis media et interna, pneumonia, torticollis, nystagmus,
conjunctivitis), Bordetella
bronchiseptica
(asymptomatic), Staphylococcus
aureus,
Pseudomonas
aeruginosa,
Listeria
monocytogenes,
Microsporum
canis,
Trichophyton
mentagrophytes,
Sarcoptes
scabiei
(sarcoptic mange
: back, head, limbs and genitalia),
Salmonella
enterica,
Yersinia
pseudotuberculosis
(even asymptomatic).
,
Anaplasma
phagocytophilum
.,
PrPSc,
Otobius
megnini,
Hypoderma
bovis,
Babesia
bovis,
Babesia
divergens,
Dermatophilus
congolensis,
Bacillus
anthracis,
Brucella
melitensis biovar Abortus,
Burkholderia
pseudomallei,
Escherichia
coli O157:H7,
Coxiella
burnetii,
Leptospira
interrogans
serovar hardjo,
Anaplasma
phagocytophilum,
bovine
papular stomatitis virus,
Crimean-Congo
hemorrhagic fever virus,
Rift
Valley fever virus,
Wesselsbron
virus (WSL),
foot-and-mouth
disease virus (FMDV)
=> variant Creutzfeld-Jakob
disease (vCJD).
,
Dicrocoelium
dendriticum,
Trichostrongylus
colubriformis,
Trichostrongylus
probolorus,
Trichostrongylus
vitrinus,
Dermatophilus
congolensis,
Bacillus
anthracis,
Burkholderia
pseudomallei,
Yersinia
pestis,
Coxiella
burnetii,
orf
virus / contagious pustular dermatitis virus / ecthyma contagiosum virus,
Nipah
virus,
Tick-borne
encephalitis virus (TBEV) / Central European encephalitis virus
,
Taenia
multiceps,
Dicrocoelium
dendriticum,
Trichostrongylus
colubriformis,
Trichostrongylus
orientalis,
Trichostrongylus
probolorus,
Trichostrongylus
vitrinus,
Trichinella
spiralis,
Dermatophilus
congolensis,
Bacillus
anthracis,
Brucella
melitensis biovar Ovis,
Burkholderia
pseudomallei,
Yersinia
pestis,
Coxiella
burnetii,
orf
virus / contagious pustular dermatitis virus / ecthyma contagiosum virus,
Rift
Valley fever virus,
Louping
ill virus (LIV),
Wesselsbron
virus (WSL),
foot-and-mouth
disease virus (FMDV).
,
Yersinia
pestis,
foot-and-mouth
disease virus (FMDV),
Mycobacterium
bovis
.
.
,
Trichinella
spiralis,
Trypanosoma
brucei gambiense,
Balantidium
coli,
Brucella
melitensis biovar Suis,
Mycobacterium
bovis,
Burkholderia
pseudomallei,
Leptospira
interrogans serovar pomona,
pseudorabies
virus (PrV) / Aujeszky's disease virus (ADV) / suid herpesvirus 1,
Nipah
virus,
Influenzavirus
A H1,
Influenzavirus
A H3,
Influenzavirus
A H4,
Influenzavirus
A H7,
Influenzavirus
A H9,
Japanese
encephalitis virus (JEV),
Hepatitis
E virus (HEV)
(1.9% of livers).
,
Taenia
solium,
Yersinia
pestis,
Trichostrongylus
vitrinus
,
Pongola
virus
,
Dermatophilus
congolensis,
Bacillus
anthracis,
Clostridium
botulinum serotype B,
Clostridium
perfringens serotype C,
Rickettsia
rickettsii,
Burkholderia
mallei,
Anaplasma
phagocytophilum,Burkholderia
pseudomallei,
Leptospira
interrogans,
Pongola
virus,
Influenzavirus
A H3,
Influenzavirus
A H7,
Japanese
encephalitis virus (JEV),
West
Nile virus (WNV),
EEEV,
Venezuelan
equine encephalitis virus (VEEV),
Western
equine encephalomyelitis virus (WEEV).
,
SFV
,
Vesicular
stomatitis virus serotype Chandipura
.
,
yellow
fever virus,
Hepatitis
E virus (HEV)
- marmosets : lymphocytic choriomeningitis virus (LCMV)
is the main human pathogen associated with dog bites.
,
is conferred evolutionary advantage if its human host is incapacitated,
because a healthy human easily could evade a mosquito, the flight speed
of which is estimated at 5 to 7 Km/h. Incapacitation of the host therefore
increases the feeding opportunities for the mosquitoes and perpetuates
the epidemic and enzootic cycles of malaria. In such a system, the vectorial
capacity (VC) = ma (P/F)(e-n/E)E where :
.
microflora caused by host metabolism changes),
becomes pathogenic.|
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ingestion of certain bacteria or fungi by amoebae (the host) can be beneficial to the amoebae, as the microorganisms are a source of food, and detrimental to the ingested microorganism |
|
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human intestinal flora synthesizes vitamin K and the host provides a niche with nutrients |
|
|
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interactions that can result in microbial pathogenesis :
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establishment of microbial infection in dead-end hosts (eg. cysticercosis) |
,
Staphylococcus
spp.,
and Streptococcus spp.
and Clostridium perfringens)
and parainfluenzaviruses,
Vibrio
cholerae
and Shigella dysenteriae))
triggers the release of inactive plasminogen
(normally stored by the body until it is needed), washing away the barriers
that keep the infection at bayref.
GAS cause serious problems only in a few patients due to differences in
genes for plasminogen. Mus musculus is normally so resistant to
GAS as mouse plasminogen is different from the human form, and is not targeted
by the streptokinase; GAS cause only localized infections when injected
under the skin of a mouse, because its enzyme is not equipped to make blood
clots break down. MRSA, which causes such a serious problem in hospitals,
also relies on an enzyme that activates plasminogen)
(a toxin), Streptococcus
spp.(streptolysin)
and various Clostridium
spp..
May be channel-forming proteins, phospholipases (e.g. produced by Clostridium
perfringens
(a toxin)) or lecithinases (e.g. produced by
Clostridium
perfringens)
that destroy RBCs and other cells (i.e., phagocytes) by lysis.,
HHV-2
/ HSV-2,
HHV-4
/ EBV,
HHV5
/ CMV.
is an exception in that it doesn't bind to cholesterol but rather to CD59
prevents internalization of GAS into lysosomes and intracellular killing
by pharyngeal epithelial cellsrefexotoxins)
is responsible for the clinical manifestations of meningitis
production, as is observed in patients who have had Mycobacterium
tuberculosis
: ADE-mediated ligation of FcRs might suppress host-cell antiviral gene
expression by promoting early IL-10 secretion, resulting in the expression
of SOCS proteins and a Th2 bias (e.g. Ross
River virusref1,ref2)
(complement-dependente ADE), e.g. C1q)refref1,
ref2ref
serotypes can be explained in the light of a process of antibody-dependent
enhancement (ADE) leading to increased mortality. If enhancement is sufficiently
great, a substantial immunological distance is necessary for 2 serotypes
to stably coexist in the populationrefrefrefref
with minimum or no risk for ADE. It is also used for antibody-mediated
targeting of gene therapy vectors.
pneumonia
infectionref),
hydrophobia,
Pneumocystis
carinii,
Saccharomyces
cerevisiae),
Haemophilus
influenzae,
Neisseria
meningitidis,
Cryptococcus
neoformans,Candida
albicans,
Arboviruses, Toxoplasma
gondii
: notably, each also has a polysaccharide capsule that is the key determinant
of their capacity to induce host damage, and each causes a similar clinical
syndrome),
Mycobacterium
tuberculosis,
HSV-1,
HIV-1),
vaccinia
virus),
Mycoplasma
pneumoniae,
mumps
virus,
Chlamydia
trachomatis,
Trypanosoma
spp.)
?, SARS coronavirus?,
Tropheryma
whipplei,
theoretical agents that cause non-infectious diseases). The dashed line
below the x-axis in the panel for Class 6 reflects recent evidence that
H.
pylori can confer a benefit in certain hosts, based on the observation
of an inverse correlation between colonization with this organism and GERD.Following infection by the microorganism, 4 main outcomes, or states, are possible :
b | a microbial factor is entirely responsible for host damage — for
example, a toxin that causes damage irrespective of the host response because
toxin action is so rapid and/or the amount of toxin is insufficient to
trigger an immune response.
c | the Class 4 curve is extended below the x-axis. Such a theoretical
microorganism would be a commensal in the setting of intermediate host
responses, but pathogenic in hosts with either weak or strong responses.
d | the inverted parabola represents a putative host–microorganism
interaction that induces damage over a narrow and limited range of responses,
but not in the presence of either strong or weak host responses. One example
of such a phenomenon would be an antibody response to a hypothetical microorganism,
whereby host damage is caused by antigen–antibody complexes. Although we
cannot think of a specific microorganism that fits this description at
this time, examples of this type of host damage are the host–microorganism
interactions characterized by the Jarisch-Herxheimer
reaction
following treatment of syphilis, the similar reaction that can occur after
the initiation of therapy for Pneumocystis
cariniipneumonia,
and serum sickness
following the injection of foreign protein.
These states are a consequence of the outcome of the amount of host
damage that results from host-microorganism interactions over time, and
are generally continuous, such that when damage exceeds a threshold amount,
another state becomes relevant. The use of damage as the common classification
for microbial pathogenicity and virulence simplifies the lexicon of microbial
pathogenesis and makes it possible to discard ambiguous terms, such as
commensal, saprophyte, opportunist, exposure, and carriage.
Host damage-time plots : e.g.
and echoviruses
(see also original
antigenic sin (OAS))
against antigens of an infectious organism. IgM antibodies directed against
specific viral antigens can be detected due to nonspecific polyclonal activation
of memory cells from a previous infection with an unrelated agent. Immune
cells may became activated during viral infections or immune diseasesref1,
ref2,
ref3,
ref4.ref,
HHV-3
/ VZVref,
HHV-4
/ EBVref,
HHV-5
/ CMVref,
parvovirus
B19ref
and HAVref.
Low-avidity antibodies are detected in cases of acute infection, whereas
high-avidity antibodies are present in subjects with a history of prior
infection. The normal immune response includes maturation from low- to
high-avidity antibodies that are maintained for life.,
which can be longer or shorter than incubation period. Titre must increase
> 4 folds between acute phase and convalescence (> 2 weeks, 10-20 days)
to have a diagnosis. It is used for :
'rumour surveillance' : public-health experts are poised to exploit an unlikely weapon in the war against bird flu and other fatal diseases. They want to expand a worldwide system for eavesdropping on rumours. Listening to gossip may sound like a flimsy means of spotting potentially devastating microbes and viruses. But the World Health Organization (WHO) already uses 'rumour surveillance' to monitor online media for early signs of epidemics, including ebola, cholera and severe acute respiratory syndrome (SARS). Epidemiologist Gina Samaan of the WHO's Western Pacific Regional Office in Manila and her colleagues examined whether a 2004 effort to detect rumours of bird flu helped combat the disease as it whipped through poultry flocks in Asia. Of 40 rumours from websites, newspapers, e-mails and experts, 9 were found to be true, and several prompted action that may have helped to stem the disease's spreadref. For example, initial reports of duck deaths in China were later confirmed to be avian influenza, and prompted over 40 countries to ban imports of poultry from China. Traditionally, the beginnings of a disease outbreak have been picked up by medical clinics and reported to government agencies, who in turn inform the WHO. But this can be slow, because many countries lack the resources to monitor and report diseases properly and the system can get bogged down in bureaucracy and politics. The spread of electronic communication and the Internet opened up a comprehensive and speedy way of scanning the globe for disease. To take advantage of this, the WHO set up its rumour surveillance network in 1997. The mainstay of the system is a sophisticated search engine called the Global Public Health Intelligence Network, based in Canada. It continuously scans and filters all news wires and online media reports for keywords such as 'outbreak' and 'epidemic' in 6 languages, ranging from English to Arabic. A team of experts checks whether the hits are really outbreaks of international concern, based on the severity of the disease and the credibility of the source. This information is passed to WHO experts in regional offices around the world, who may ask the country involved for verification that the disease is real and then help them to tackle it. The WHO compiles its own figures on the effectiveness of its rumour surveillance. From the tens of thousands of initial reports detected between January 2001 and October 2004, the system picked up around 1,300 disease outbreaks of potential global importance : of these, 850 proved real. The WHO now wants individual countries to set up rumour surveillance systems that would run alongside the WHO's international one. These could filter reports according to different criteria that might be better at unearthing local incidents and diseases that are important to a particular country. The establishment of such national systems is increasingly urgent because of the possibility that avian flu might spread into humans and trigger a pandemic. Many countries may be pushed to introduce rumour surveillance if an updated set of rules, called the International Health Regulations, which are likely to be adopted at the WHO's World Health Assembly in May, comes into effect later in 2005 requiring member countries to carry out real-time surveillance for a plethora of diseases and report potential emergencies to the rest of the world. biocontainment patient care unit (BPCU)ref
)
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