section)
Table of contents :
Thousands of different commensal
microbial species populate Homo
sapiens outer and inner body surfaces :
108 bacteria/ mL
103-105 bacteria per gram or mL of luminal contents
in mice, consisting mainly of acid-tolerant species (e.g. Lactobacilli
spp., Streptococcus spp., Helicobacter
pylori) unless patient is treated with antiacids (H2
antagonists,
PPI),
a risk factor for aspiration
pneumonia
500-1,000 different species exist : their microbiome contains 100-fold
more genes than human genome. Gut is colonized ~ 40 hrs after birth.
108 bacteria / mL : Döderlein's bacillus
: one of the gram-positive rods commonly found in vaginal secretions that
may consist of mixtures of Lactobacillus acidophilus, L. casei,
L.
cellobiosisus, L. fermentum, or Leuconostoc mesenteroides.
Said by some to be identical with
L. acidophilus
microbiota is dominated by Corynebacterium
spp., Microbacterium spp., Rhodococcus
spp., Staphylococcus epidermidis,Staphylococcus
capitis, Staphylococcus hominis,Staphylococcus
haemolyticus,Staphylococcus
lugdunensis and Staphylococcus
warneri. Under special circumstances, single species, including
IgA1
protease-producing bacteria, may become predominant in a restricted area
of the nasal mucosaref.
commensals can be divided into,
being present on 31 % of physicians' hands (7.104 CFUs
/ hand) and 17 % of nurses' hands (4.104 CFUs / hand).Taxonomic units
);
strictly or facultative anaerobes => endogenous infections)
(chronic granuloma with draining fistulae from which sulfur granules
come out)
or mucosal injuries-using
females or after trauma,
caries,
gingivitis
with a rash that may look like scarlet fever, the spectrum of diseases
caused by A. haemolyticum has been expanded to include invasive
infections, including sepsis and osteomyelitis. The pathophysiology of
the rash is unknown;
)
at the pear-shaped end ; resist high [K2TeO3], reducing
it to Te (gray-black precipitates; Chinese ideograms-shaped colonies).
Core regions containing cell wall components contributing to pathogenicity
have been identified, including an arabinogalactan polymer involved in
adhesion.,
oropharyngitis
(oedema => "bull-neck") and/or
larynx (maximal vascularization => maximal toxin absorption => malignant
angina) or tracheitis (croup
: suffocating risk if detachment occurs !) with regional lymphadenitis.
Complications : after 2÷3 weeks 20÷30% undergo bacteraemia
=>
and ciliary nerve paralysis, which manifest as strabismus, blurred vision,
or difficulty with accommodation.
Paralysis of the diaphragm can ensue.
that don't undergo scaring
looking for tox gene
within 48 hours of onset (almost useless after day 4) after testing for
sensitivity to antitoxin;
G 600,000 units IM bid for 14 days (150,000 units/kg/day IV for 10 days
for pediatric patients) or erythromycin
500 mg parenterally or po qid,
toxoid
or heterologous
vaccine in newborns : diphteria is reemerging in countries which have stopped
vaccination programmes. Concentration of neutralizing Abs
may be evaluated by Schick test (1913):
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ref1,
ref2
result from chronic inflammationref;
cord
factor
of virulent mycobacteria that prevents fusion of lysosomes with endosomal
vacuoles and allows serpentine cord-like formation in vitro, while
in
vivo they occur as "swallow tail-shaped" ; produce exochelin-mycobactin
system for Fe2+ uptake; colonies will normally grow in 2-3 weeks,
but if a patient is on some kind of chemotherapy, then growth may take
up to 8 weeks. At 37 °C, cultures have been found viable and virulent
after 12 years of sctorage. After 2 hours of direct sunlight, organisms
from cultures will die. If the bacillus is contained within the sputum,
it will take 20 to 30 hours of direct sunlight before the organisms are
killed. Tubercle bacilli can survive for several months in sputum if protected
from direct sunlight.
(5), breast lift (4), breast reduction (4), and breast implant (1). Symptoms
of infection began a median of 5 weeks after surgery (range: 1-20 weeks)
and included subcutaneous or deep-tissue abscesses requiring incision,
drainage, and antibiotic therapy in all patients; 9 patients were hospitalized.
Molecular typing using PFGE and randomly amplified polymorphic DNA PCR
confirmed that M.abscessus isolates from 7 of 12 specimens were
indistinguishable. Organisms with this common genetic pattern were recovered
from patients who had surgery performed during Oct-Dec 2003 in the same
surgical center in Santo Domingo.
and crystalline keratopathy : therapeutic lamellar keratectomy with flap
removal can provide an effective treatment modality for the management
of post-LASIK keratitis
that is unresponsive to amikacin and ciprofoxacin given for 6 weeks
,
imipenem-cilastatin,
panipenem,
meropenem,
clarithromycin
and minocycline
in ruminants and other animals
: the involvement of MAP in Crohn's disease (CD) in humans has been uncertain
because of the substantial difficulties in detecting this pathogen : in
its Ziehl-Neelsen staining-negative form, MAP is highly resistant to chemical
and enzymatic lysis. By using optimized sample processing and DNA extraction
procedures, MAP is detected by nested PCR methodologies targeted at IS900
in 92% of fresh ileocolonic biopsy specimens from patients with CD vs.
26% of patients in a control group and by mycobacterial growth indicator
tube (MGIT) cultures in 42% CD patients (60% when incubated for > 38 weeks)
vs. 9% of controlsref.
Up to 55% of dairy herds in Western Europe and America are infected with
the bacteria, which can survive the normal flesh method of pasteurisation
(it involves heating milk to 72°C for 15", but to be sure of killing
MAP milk would need to be heated to that level for 30") and MAP bacteria
are present in 2% of retail pasteurised milk cartons : those individuals
with CD or their close relatives, who may feel particularly at risk, should
drink UHT milk. Water supplies
become infected as the droppings from herds seep into the soil, down into
natural aquifers. American studies have isolated MAP from the breast milk
of women with Crohn's disease but not in women who do not have the illness.
: MAP inflames the nerves of the gut in both animals and humans
are rarely infected by M. bovis but are commonly infected via environmental
contamination by the avian/intracellulare complex, which does not spread
between pigs.
=> opportunistic disseminated infection in patients with AIDS
=> rare pneumonia
(sometimes cavitating) in patients with COPD
or CF
=> carpal
tunnel syndrome (CTS)
(monolateral cervical
lymphadenitis)
in children from ingestion of milk, fresh milk derivatives or mollusks
=> fibrosis, ulcer
and fistulae
: at T > 84°F, where many tubs operate, chlorine loses its disinfectant
properties, and MAC can flourish. The bubbles and steam arising from the
tub create an aerosol through which MAC readily enters the lung by inhalation.
. Discontinuation of hot tub use, without antimycobacterial therapy, leads
to prompt improvement in symptoms, pulmonary function, and radiographic
abnormalities, strongly supporting a diagnosis of hypersensitivity pneumonitis.
,
bones (carpal
tunnel syndrome (CTS)),
CNS, prosthetic heart valves, skin and soft tissues, including localized
infections and abscesses at the site of puncture wounds
),
CNS, prosthetic heart valves, skin and soft tissues, including localized
infections and abscesses at the site of puncture wounds
,
painful swelling, ulcers
progressing into abscess), septic
arthritis,
osteomyelitis,
and pneumonitis in patients who are immunologically compromised and submandibular
lymphadenitisref1,
ref2,
ref3,
ref4,
ref5,
ref6
and draining fistulas in apparently immunocompetent children. Underlying
conditions in the compromised patients have included AIDS; renal, bone
marrow, and cardiac transplantation; lymphoma; rheumatoid arthritis; marrow
hypoplasia; and Crohn's disease
,
clarithromycin,
rifabutin,
and rifampin.
Timely diagnosis and therapy require communication between clinician and
the laboratoryref
),
a chronic pneumonia
involving the upper lobes, with evidence of scarring. Rare disseminated
infection in immunocompromised hosts.
(carpal
tunnel syndrome (CTS),
synovitis,
tendinitis,
osteomyelitis)
in young European children, while isolations from other sites (lung specimens
included) were described only in immunocompromised patientsref1,
ref2,
ref3,
ref4,
ref5,
ref6,
ref7
: anyway a chronic pulmonary M. lentiflavum infection in an elderly
immunocompetent woman has been reportedref
(prevalence : 7%; => lepromatous lepromatous leprosy), gibbons and Erinaceidae.
Transmission of leprosy remains poorly understood, with nasal droplet infection,
contact with infected soil and insect vectors thought to play a role. Not
culturable in vitro : propagated by injection into the footpads
of Mus musculus
or Rattus norvegicus
(lower T)
: infection of nasal epithelium (it exits from the phagosome before phagolysosome
formation) => incubation ranges from 3 months to 40 years (average 2-5
years for tuberculoid form and 8-12 years for lepromatous form !) => type
II hypersensitivity
due to cross-reactivity between bacterial and skin Ags presented on HLA-DRB1*15
(in HLA-DR2 haplotype)
in 25-50%. Serological status is controlled
after lepromin subcutaneous injection :
after 3÷4 weeks (primary immune response)
(side effects : diffuse
skin hyperpigmentation,
unaccepted by Hinduists), clofazamine
and rifampin
daily for at least 2-3 years until all biopsies are negative for acid-fast
bacilli. Patients with undeterminated or tuberculoid leprosy may be treated
with dapsone and rifampin as above for 6÷12 months, followed by
dapsone alone for > 2 years. Type III hypersensitivity is treated with
prednisone
or thalidomide.
=> wart => aquarium fish or swimming pool granuloma, usually of
the skin and soft tissues.
(carpal
tunnel syndrome (CTS)),
osteomyelitis,
chronic
laryngitis.
.
None of these cases was fatal. A fatal case rapidly progressive dementia
was reportedref
but aetiology was doubtfulref.
(causes false positivity for urinary
tuberculosis in urinalysis), sometimes involved in pulmonary, skin,
soft-tissues and bone infections.
similar to tubercular pneumonia
and Diplonychus spp.),
which were able to transmit M. ulcerans to mice by their bites,
suggesting a possible mechanism for human infectionref.
Another study reported a potential role for fish in transmissionref.
Fish were found positive for M. ulcerans DNA, and all appeared to
feed on insects or plankton and were believed to concentrate M. ulcerans
from this usual food source. Endemic foci exist throughout the world, predominantly
in tropical rain forest areas. The peak incidence of the disease coincides
with the rainfall pattern and farming season in endemic districts. This
lends credence to speculation that disease onset is related to farming
activities, which predispose to injury and pricks. Mycobacterium ulcerans
has also been found in snails, spiders and crayfish. Other insects said
to have been found infected are march flies, a confusing name that may
be used for flies in the family Bibionidae
or the large biting tabanid flies (2 common genera being Tabanus
spp.
and Chrysops spp.)
: at a guess, it would seem that tabanids would be a better vehicle for
transmission of M. ulcerans. A research topic for "M. ulcerans
in Victoria"ref
says that previous research has shown that M. ulcerans ingested
by mosquito larvae can be passed to adults. Clearly if -- as it seems from
the present post -- mosquitoes serve as vectors, it needs to be known whether
transmission is mechanical (such as by infected mosquito mouthparts and/or
by their feces being scratched into the skin or abrasions) or whether the
salivary glands are infected. If transmission is mechanical, or mainly
so, then it is likely that many mosquito species might be involved, as
well as other hematophagous insects. A useful reference is a 22-page abstract
(in English) of a PhD thesis of Timothy Stinear, which has 155 referencesref.
teeming with mycobacteria
that enlarges and becomes fluctuant) with secondary skin ulceration,
leaving an undermined edge. The 3 main clinical forms are
: localized necrotizing skin ulcers; contiguous dissemination over extensive
body surfaces; and metastatic spread of M. ulcerans to distant sites,
usually skin and bone. Minor forms heal spontaneously, ordinarily in 3-6
months by a delayed-type hypersensitivity response, followed by scarring.
Devastating sequelae (scarring or amputations) often ensue from tissue
destruction and osteomyelitis.
Untreated, massive areas of skin, and, sometimes bone, are
destroyed causing gross deformities. When lesions heal, scarring may cause
restricted movement of limbs and other permanent disabilities. One important
feature of Buruli ulcer is the minimally painful nature of the disease,
which may partly explain why those affected do not seek prompt treatment.
.
,
rifampin, and fluoroquinolones). Current research findings indicate that
a combination of an aminoglycoside (amikacin or streptomycin) and rifampicin
cures Buruli ulcer in mice.
in individuals with AIDS
==bacteraemia==>
meningitis,
acute
nephritis
and pleurisy
in individuals with AIDSref1,
ref2.
Most micrococcal species, including K. sedentarius but not K.
schroeteri, were isolated from human skin and mucosa (Szczerba I, Krzeminski
Z. Occurrence and number of bacteria from the Micrococcus, Kocuria, Nesterenkonia,
Kytococcus and Dermacoccus genera on skin and mucous membranes in humans.
Med Dosw Mikrobiol 2002;55:67-74). As moxifloxacin
was more rapidly microbicidal than vancomycin in an animal model of Staphylococcus
aureus prosthetic valve endocarditisref,
it might present a potential advantage against infections caused by K.
schroeteri, especially when the oral route is favored.,
Ovis
aries,
Equus
caballus,
Canis
familiaris,
Capra
hircus,
Cervidae
which contribute to tissue injury and contributes to the inflammatory nature
of acne by inducing monocytes to secrete proinflammatory cytokines including
TNF-a,
IL-1b,
and IL-8.
Many of P.acnes 2,333 genes are involved in degrading the human
tissue as the bacterium lived off the products of this degradation.
infections
,
depending on hormonal mechanisms. The reason acne is common in adolescence
(affects up to 80% of young adults) might be because this is a time when
the skin produces more oils, which the bacterium feeds off.
ref
> second-generation tetracyclines, such as lymecycline,
doxycycline,
and minocycline,
show improved absorption (minocycline has the advantage of being rarely
associated with Propionibacterium acnes antibacterial resistance,
but can occasionally lead to potentially serious adverse effects) > trimethoprimref
at the ends of limbs
by percutaneous route
+ dapsone
or cotrimoxazole.
Surgical debridement + long-term ketoconazole
or itraconazole
is also used in treatment.
: increase in secretions, no leukorrhoea, no itching
to an inactive metabolyte
(first mainfestations in > 90%; spondylitis
in patients with HLA-B27 haplotype) => diarrhea,
steatorrhoea,
weight
loss,
fever
(54%), edema, serositis, alveolar
pneumonia,
systemic
arterial hypotension,
diffuse
skin hyperpigmentation
(54%), lymphadenitis
(54%), endocarditis
(25% => murmurs), subcutaneous nodules,
digital
hippocratism,
uveitis,
neuro-Whipple (no real meningitis,
only a subacute or chronic encephalitis : 80%), myoclonus of masticatory
and extraocular skeletal muscles (ophthalmoplegia), ataxia, paresis, hyperreflexia.
(or ceftriaxone)
and streptomycin
for 2 weeks, followed by cotrimoxazole
for 1-2 years. Jarisch-Herxheimer
reaction (JHR)
can occur.
: it doesn't occur in infected organisms.
symptomatic of inhaled anthraxref.
Although the researchers did not find a homologue to pX02—the anthracis
plasmid–containing genes that create an impenetrable capsule surrounding
and protecting the bacterium while it lies dormant in soil—they found a
different plasmid coding for a similar capsule, which may serve the same
function. Normally, when microbiologists look for anthrax, they say that
it has to be non-hemolytic and non-motile, whereas this B. cereus
isolate is motile and hemolytic. The bacillus family of bacteria is known
to be capable of gene jumping. All B. anthracis-sensitive miice
injected i.p. with the plasmid-containing B. cereus died within
14 days : anyway rabbits are a better animal model for anthrax than mice.
Moreover, injecting mice in their peritoneal cavities may not produce the
same results as making them inhale the isolate. So what they really needed
to do is get rid of that plasmid from that B. cereus isolate to
see if it was still pathogenic or disrupt the gene that encodes one of
the principal toxins
)
: nausea and
vomiting
and abdominal pain
after an incubation period of 30' to 6 hours. Occasionally,
abdominal cramps and/or diarrhea may also occur. The vomiting-type outbreaks
have generally been associated with rice products; however, other starchy
foods such as potato, pasta (pasta salada) and cheese products have also
been implicated. Food mixtures such as sauces, puddings, soups, casseroles,
pastries, and salads have frequently been incriminated in food poisoning
outbreaks.
and diarrhea
with an incubation period of 8 to 24 hours.,
meningitis,
alveolar
pneumonia,
and skin wound
infectionsref1,
ref2.
Certain populations are at increased risk for B. cereus infection,
including cancer patients, neonates, intravenous drug users, and patients
with a history of trauma, surgery, or catheterizationref1,
ref2,
ref3,
ref4.
Primary cutaneous disease attributed to B. cereus in immunocompetent
persons or in non-health-care settings rarely has been reportedref.
On 24 Aug 2004, a local health department in Georgia received a call from
a university health center describing 90 cadets with nonpruritic, impetigo-like
lesions on their scalps; B. cereus was the common organism among
the 3 patients whose lesions were cultured. The cases occurred during the
freshman military orientation week that preceded the start of the fall
term. The Georgia Division of Public Health (GDPH) conducted an investigation
to determine the source of the infections, identify associated risk factors,
and implement control measures. This report summarizes the results of the
outbreak investigation, which identified receiving a short haircut at the
start of orientation week, sharing sunscreen during the week, and membership
in Company B as strongly associated with having scalp lesions. Recommendations
to the university included changing the type of haircut required, increasing
time allowed for showering, and issuing individual sunscreen. The results
of this investigation underscore the need for military programs to incorporate
good hygiene and infection-control measures into school orientation events.
GDPH reviewed the events of orientation week, investigated cases of scalp
dermatitis, collected environmental samples, and conducted a cohort study
of participants in the military program during 4 site visits to the university.
University personnel provided a schedule of orientation activities and
a tour of each event location. Medical records from patients were reviewed
and clinical findings discussed with university health-care staff. Patients
were interviewed, and available clinical isolates were sent to the Georgia
Public Health Laboratory for confirmation. Samples, including talc, Barbicide(r)
disinfectant, and swabs of electric clippers, were collected from 2 barbershops
providing haircuts to cadets. Soil and water samples were collected from
event sites, and swabs were taken of shared helmets and sunscreen. 5 patients
donated their hats for the environmental and laboratory investigation.
CDC analyzed the environmental samples and characterized bacterial isolates
by biochemical analysis, 16S rRNA gene sequencingref,
and multilocus sequence typing (MLST)ref.
After the initial investigation, GDPH conducted a cohort study of all cadets
in the military program at the university. GDPH distributed questionnaires
to all 660 cadets, including upperclassmen, 3 weeks after orientation week.
The cadets were asked about demographic information, company and dormitory
assignment, clinical symptoms, orientation vent participation, exposure
to soil and water, and hygiene practices, including laundry, bathing, and
shared products. A case was defined as an occurrence of scalp lesions in
a cadet treated with oral cephalexin from the school health center during
10-30 Aug 2004. Measures of association were estimated using multivariate
logistic regression to control for confounding. The 4-year military program
at the university had 660 students (292 freshman and 368 upperclassmen)
organized into 7 discrete companies. Cadets lived in 5 separate dormitories,
2 per room, organized by company, sex, and class year. Each floor shared
a bathroom and a common living room. Orientation directly involved 292
freshmen; 115 upperclassmen supervised the events. Orientation started
with a short haircut for all 255 freshman males at 1 of 2 civilian barbershops.
Haircuts were performed by 1 of 8 barbers in random order using electric
clippers without a scalp guard. The 3rd day of orientation week, the cadets
completed an obstacle course involving immersion in mud and river water.
On the final day, participants were required to rappel from rock walls
and participate in survival training exercises. Helmets were worn and sunscreen
was shared among cadets during these activities. 94 (14%) of 660 cadets
had scalp lesions, and 1 cadet was infected twice during the period from
the start of orientation to when the questionnaire was administered. 33
patients sought care at the student health center on the 4th day of orientation
week, and 57 sought care on the 5th day. 5 more cases, including the recurrent
case, occurred 1 week after the start of school. All patients participated
in orientation week; all were male and ranged in age from 16 to 24 years.
The majority of patients were freshmen (84/94; 89%) and received a haircut
on the 1st day of orientation (89/94; 95%). Approximately 1/3 of the patients
(33/94; 35%) were in Company B. The index patient noted onset of symptoms
on the 3rd day of orientation. Yellow sticky discharge followed by honey-colored
crusts on the crown of his head were noted. Lesions were nonpruritic. Other
patients had similar lesions with the same distribution. Infections resolved
within 48 hours with the use of antibacterial soap and oral cephalexin
(5-day prescription). Health care providers obtained samples for culture
from lesions of 3 cadets. B. cereus was the only common organism
isolated from all 3 patients and was identified by using biochemical tests
and 16S rRNA gene sequencing. When analyzed by MLST, all 3 clinical B.
cereus isolates were indistinguishable. B. cereus also was cultured
from 2 separate barbershop clippers (2 isolates), soil from the school
grounds and orientation events (5 isolates), and helmets (2 isolates) worn
during rappelling exercises. 5 environmental isolates (3 soil samples and
2 clippers) matched the clinical isolates by 16S rRNA. MLST was performed
on these isolates, resulting in 4 unique sequence types (3 from the soil
samples and 1 from the 2 clippers), with no matches to the clinical B.
cereus sequence type. The response rate for the cohort study was 73%
(483/660); the response rate for freshmen was 84% (248/292). Of the respondents,
423 (88%) were male, and 248 (51%) were freshmen, which was representative
of the entire cohort. The median age was 19 years, and 405 (84%) cadets
were white. After adjusting for sex, freshman class status, and participation
in orientation week, the multivariate logistic regression model indicated
a statistically significant association between having scalp lesions and
receiving a haircut (adjusted odds ratio [AOR] = 10.6), membership in Company
B (AOR = 9.7), and sharing sunscreen (AOR = 2.7). Other risk factors examined
included demographic information, exposure to soil and water, and hygiene
practices (e.g., laundry, bathing, and use of shared products). B. cereus
is a recognized bacterial pathogen in humans. Non-gastrointestinal infections
are usually the result of a breakdown in natural protective barriers such
as the skin or immune systemref1,
ref2,
ref3.
The findings in this report indicate that immunocompetent persons can be
vulnerable to cutaneous B. cereus infections when skin is compromised.
Isolation of 3 indistinguishable B. cereus isolates from 3 patients
on 2 separate days suggested that this was a common-source outbreak and
not a laboratory contaminant, even though the environmental source of B.
cereus was not identified during the investigation. All but 5 cases
were diagnosed on 2 concurrent days, making person-to-person transmission
unlikely. Transmission most likely occurred from an exposure at the beginning
of the orientation week. The short haircut likely caused microabrasions,
compromising the protective effect of scalp epidermis. Exposure to mud,
sun, and sunscreen further provided an environment suitable for bacterial
growth. The findings in this report are subject to at least 3 limitations.
First, only 3 clinical samples were available for culture. Because of the
number of cases and the positive response to therapy, the health-center
staff treated cases empirically before GDPH involvement. Second, other
risk factors and potential confounders might not have been identified during
the site visits. Finally, cadets were asked about their orientation exposures
nearly 3 weeks after the events occurred; recall bias might have influenced
the findings. As a result of this investigation, GDPH made recommendations
to the university military program for future orientations to minimize
the risk for another outbreak. These included 1) changing the type of haircut
required for male cadets that would allow for more hair and less injury
to the scalp, 2) allowing adequate time for personal hygiene, and 3)
distributing individual packets of sunscreen and discouraging sharing of
sunscreen. These recommendations were implemented during the 2005 orientation
activities; no skin infections were reported. University military programs
should establish infection-control practices including good hygiene as
part of their organized orientation events. Since many laboratories may
not identify B. cereus from a skin culture and refer to it as Bacillus
species -- which may well be thought of as a contaminant from a typical
staphylococcal-streptococcal impetigo -- sporadic cases may indeed occur.
Reference 7 above describes a 29-year-old with a chronic (2-month) leg
ulceration that initially developed during a 3-month stay in French Polynesia
and developed into a superficial ulceration with dark, adherent eschar
and surrounding erythematous halo. The culture was obtained from
a biopsy instead of a swab and revealed a pure culture of B. cereusref
and acute
liver failureref1,
ref2
episodes. In 2004, the CDC reported 2500 cases across the country and 500
deaths.
),
and raw and smoked fish. Its ability to grow at temperatures as low as
3°C permits multiplication in refrigerated foods. Expecially frequent
in immunosuppressed individuals, alcoholists, pregnants and newborns. The
greatest threat of listeriosis is from ready-to-eat products that do not
require further cooking at home. L. monocytogenes in raw food that
will be cooked before consumption is less of a concern to the food industry,
since the bacteria are killed during cooking. Listeriosis can be acquired
from seafood, although most think of the risk from processed deli meats
1st. Yearly, recalls of seafood, especially smoked salmon, are posted on
FDA's website. Although not generally linked to large outbreaks, those
at high risk, such as pregnant women and those individuals with compromised
cell-mediated immunity, should avoid the food described below. L. monocytogenes
has been isolated from raw fish, cooked crabs, raw and cooked shrimp, raw
lobster, surimi (minced, processed fish used in the preparation of imitation
seafood, especially imitation shellfish) and smoked fish (Ward D, Bernard
D, Collette R, et al. (Eds.): Hazards Found in Seafoods, Appendix III.
In HACCP: Hazard Analysis and Critical Control Point Training Curriculum,
2nd ed., p. 173-188. UNC-SG-96-02. North Carolina Sea Grant, Raleigh, NC,
1997).
=> Listeria-induced placental and fetal necrosis with unrestricted bacterial
multiplication, increasing the incidence of postimplantation loss and
poor pregnancy outcome (intrauterine and neonatal death, abortion,
stillbirth or severe neonatal infections similar to neonatal Group B Streptococcus
sepsis, with early and late onset forms of disease)
or cotrimoxazole
is possible, and preterm delivery may be avoided
(Listeria neuromeningitis), due to the elective location of foci
of subacute infection and inflammation in the brain stem by intraaxonal
(unilateral) bacterial spread from peripheral sites to the ipsilateral
CNS : listeria rhombencephalitis
(50%). The disease has a characteristic biphasic course: a nonspecific
prodrome of headache, nausea
and vomiting,
and fever lasting for a several days is followed by progressive and persistent
asymmetrical cranial-nerve palsies (sometimes complex auditory hallucinations;
rarely central apnea with simultaneous consciousness impairment due to
pons and medulla lesions of the reticular formation)with
pharyngitis,
mononucleosis and subacute endocarditisref
and gentamicin
or, for patients who are intolerant of b-lactam
agents, cotrimoxazole
extracts added to meat : the flavor cannot be totally eliminated because
some intensity of flavor is linked to the compounds that are inhibitory
and bacteremia,
and rarely with arthritis, spondylodiscitis,
meningitis,
brain
abscess
and septic shock.
Liver
abscess
is very rare, and only a few cases have been reportedref.
due to continuous ambulatory peritoneal dialysis
in individuals with prosthesis
,
skin and soft-tissue infections, infant staphylococcal septicemia
due to continuous ambulatory peritoneal dialysis
-resistant
.
and asymptomatic bacteriuria
due to continuous ambulatory peritoneal dialysis, abscessesref,
meningitisref,
ventriculoperitoneal shunt infectionref,
spondylodiscitisref,
prosthetic joint infectionref,
catheter-related bacteremiaref,
and endocarditisref.
Infections with S. lugdunensis tend to have a more fulminant course,
with an outcome resembling that of S. aureus infections rather than
that caused by coagulase-negative staphylococciref.
In addition, these organisms are frequently misidentified as S. aureus
because
of their morphologic appearance with yellow pigmentation and complete hemolysis
when cultured on blood agar. A case of a device-related bloodstream infe
due
to continuous
ambulatory peritoneal dialysis
.
and asymptomatic bacteriuria
,
intravenous catheter-related septic
shock
due to continuous
ambulatory peritoneal dialysis
,
erythromycin,
chloramphenicol,
neomycin,
ciprofloxacin
and vancomycin
(but vancomycin-intermediate strains have been reported) and resistant
to gentamicin,
clindamycin,
rifampin,
methicillin,
ampicillin
and ceftriaxone.
due to continuous
ambulatory peritoneal dialysis
and asymptomatic bacteriuria
,
endocarditisref,
and multifocal discitisrefref,
brain
abscessref
.
ref.
Infective discitis due to enterococci has been reported on 6 previous occasions
since 1969, each one associated with advanced ageref
infections => septicemia
=> subacute endocarditis,
pyogenic
liver
abscess
: enterococcal meningitis is an uncommon disease accounting for only 0.3%
to 4% of cases of bacterial meningitis which is nevertheless associated
with a high mortality rate. It has been described most frequently in patients
with neurosurgical conditions (i.e. head trauma, shunt devices, or CSFd
leakage), although it can also occur as a "spontaneous" infection complicating
remote enterococcal infections such as endocarditis or pyelonephritisref.
Enterococcus
faecalis and Enterococcus faecium are the 2 species most frequently
isolated during the course of meningitis (76–90% and 9–22% respectively)
with a poor visual prognosisref1,
ref2.
They are, however, rarely identified in endogenous endophthalmitisref1,
ref2,
ref3.-resistant
Enterococci
(Van A strain VRE, expecially vancomycin-resistant
Enterococcus
faecium (VREF)) thanks to 57.9 kb multiresistance, conjugative
plasmid with vancomycin resistance encoded in the integrated mobile genetic
element Tn1546 (first detected in 1988) => mortality = 37% vs. 16% in VSEref.
Following their initial recognition in a south London hospital in 1987,
vancomycin-resistant enterococci (VRE) had been isolated in at least 71
UK hospitals by 1995ref.
They are an even greater problem in the USA, and have been isolated in
many other countries. Although 85–90% of clinical isolates of enterococci
are Enterococcus faecalis, most VRE are Enterococcus faeciumref.
After allowing for the effect of blood, which raised the MICs of quinupristin/dalfopristin
four-fold, 98.3% of E. faecalis isolates and all the Enterococcus
avium, Enterococcus casseliflavus and Enterococcus gallinarum
appeared resistant to quinupristin/dalfopristin,
whereas 98.8% of the E. faecium isolates and the single Enterococcus
raffinosus isolate were susceptibleref.,
commensal in vagina
=> pleural empyema..
ChoP can be bound by CRP.
Lancefield
classification of b-hemolytic Streptococci
(1933) : a serologic classification of the hemolytic streptococci, based
on extraction and examination by a precipitin technique of group-specific
carbohydrate antigens contained in the cell wall. 18 serotypes / groups
(A-H and K-V) can be distinguished (please note that for A-C, E-H, K, L,
O and R serotypes the Ag determinant is contained in C-polysaccharide,
while for D and N it is a teichoic acid and it is unknown for the remaining
serotypes !).
on keratinocytes
=> blocks the binding of complement to the underlying PGN => prevents PMN
phagocytosis-mediated
signaling. Invasion associated gene (iagA), which encodes a glycosyltransferase
homolog required for synthesis of glycolipid diglucosyldiacylglycerol,
a cell membrane anchor for LTA, is required for human brain microvascular
endothelial cells invasion in vitroref,
sulfonamides
or cotrimoxazole.
,
endocarditis,
alveolar
pneumonia,
endometritis,
otitis
media,
meningitis,
septic
arthritis
within 48 hrs (lethality 50%)
within 2 months (lethality : 20÷30%)
after 6-7 days incubation
after 6-7 days incubation
(an inhibitor of the MAC of human complement) via residues that are the
binding site for the C8a and C9 complement proteinsref.
(?)
,
lung
abscess
and cerebral abscess
=> peritonitis
after 6-7 days incubation
process initiated by S.sanguinis.,
serotype XIV is cross-reactive with human blood group Ag A.
protease (monomers and dimers)
by types 1, 3, 6, 7, 12, 14, 16, 18, 19 and 23..
Sequelae :,
pleural
effusion,
pleural
empyema
/ pneumococcemia => invasive pneumococcal disease (IPD) : endocarditis,
septic
arthritis,
acute
liver failure,
ileus,
conjunctivitis,
acute
otitis media
(66% of those before age 4, 50% of those before age 6; expecially from
types 6, 14, 19 and 23; if untreated may lead to perforation with 40% lethality),
myringitis,
parotitis,
mastoiditis,
sinusitis
=> meningitis
(the most common bacterial meningitis in adults), Waterhouse-Friderichsen
syndrome (WFS)..
A 9-valent pneumococcal conjugate vaccine, PncCV, prevents 31% (95% confidence
interval = 15–43%) of pneumonias associated with any of 7 respiratory viruses
in children in hospitalref.
Worldwide, most antibiotic-resistant infections are caused by 5 of the
7 serotypes in the 7-valent pneumococcal conjugate vaccine (PCV-7)
(6B, 9V, 14, 19F, and 23F)ref.
A second major direct effect of PCV-7, which was not specifically anticipated,
has been a reduction in nasopharyngeal carriage of vaccine strainsref.
Strains targeted by the vaccine were those that had been most commonly
isolated in young children; they were also strains that had been most consistently
exposed to the pressure of antibiotic overuse and, therefore, the most
likely to be resistant to antibiotics. In 1998, 24% of invasive pneumococcal
isolates in the USA were nonsusceptible to penicillin, and these five serotypes
comprised 78% of such strainsref.
Modeling predicted that in the absence of a pneumococcal conjugate vaccine,
the proportion of pneumococcal strains that were nonsusceptible to both
penicillin and erythromycin could reach 41% by 2004ref.
Because of the association between serotype and resistance, the conjugate
vaccine would be expected to reduce the incidence of disease caused by
resistant strains, even though the vaccine is designed to induce antibodies
against certain capsular types. Whether vaccine use would induce the emergence
of serotypes that were typically not resistant as clinically significant
causes of resistant infections was unknown. In addition, the possibility
that use of a vaccine that targets only 7 of 90 pneumococcal serotypes
would lead to an increase in disease by nonvaccine types (so-called replacement
disease) was a concern. Rates of invasive disease caused by penicillin-nonsusceptible
strains and strains not susceptible to multiple antibiotics peaked in 1999
and decreased by 2004, from 6.3 to 2.7 cases per 100,000 (a decline of
57%; 95% confidence interval, 55 to 58%) and from 4.1 to 1.7 cases per
100,000 (a decline of 59%; 95% confidence interval, 58 to 60%), respectively.
Among children under 2 years of age, disease caused by penicillin-nonsusceptible
strains decreased from 70.3 to 13.1 cases per 100,000 (a decline of 81%;
95% confidence interval, 80 to 82%). Among persons 65 years of age or older,
disease caused by penicillin-nonsusceptible strains decreased from 16.4
to 8.4 cases per 100,000 (a decline of 49%). Rates of resistant disease
caused by vaccine serotypes fell 87%. An increase was seen in disease caused
by serotype 19A, a serotype not included in the vaccine (from 2.0 to 8.3
per 100,000 among children under < years of age). In addition to reductions
in the rates among young children, reductions > 50% in the rates of
invasive disease caused by resistant strains were documented among older
children and adults, who would not have received the conjugate vaccine
("herd effect"). With all age groups considered together, the estimated
number of cases caused by strains with reduced susceptibility to penicillin
or multiple antibiotics fell by half after the introduction of the conjugate
vaccine. Studies of adults have shown that exposure to children can increase
the risk of colonizationref
and invasive diseaseref.
Conjugate pneumococcal vaccines have been shown to reduce the risk of carriage
and transmission of vaccine-type strains among vaccinees and their household
membersref.
The change that we observed in the rate of resistant disease among adults
was due to a reduction in disease caused by vaccine serotypes — a finding
suggesting that the vaccine interrupts the transmission of resistant pneumococci
from children to adults. No reduction in the incidence of resistant
disease caused by serotypes included in the 23-valent polysaccharide vaccine
but not in the 7-valent conjugate vaccine was found (data not shown);
therefore, it appears that the decline in invasive antibiotic-resistant
disease among adults was not linked to an increase in the use of the polysaccharide
vaccine. Polysaccharide-vaccine coverage among adults 65 years of age or
older increased from 54% in 1999 to 64% in 2003ref1,
ref2.
An increase in resistant disease caused by nonvaccine types (so-called
replacement
disease) was found, but the magnitude of this effect was relatively
small. Most resistant infections from serotypes not in the vaccine were
caused by serotypes 6A and 19A. A drop in the rate of disease caused by
serotype 6A and a concurrent increase in the rate of disease due to serotype
19A suggest, as previously reported, that the 6B vaccine component provides
cross-protectionref1,
ref2,
ref3
against serotype 6A disease but that the 19F component does not protect
against 19A diseaseref1,
ref2.
The increase in resistant disease caused by serotype 19A is a concern.
Serotype 19A is often resistant and is a common cause of respiratory tract
infectionsref1,
ref2.
It is difficult to predict whether the increase in resistant serotype 19A
or other serotypes not covered by the vaccine will continue. Nevertheless,
this replacement disease has the potential to reduce the overall benefit
of the vaccine against resistant infectionsref.
According to estimates of U.S. vaccine coverage, only 73% of children 19
to 35 months old in 2004 had received at least 3 of the recommended four
doses of conjugate pneumococcal vaccineref.
; by the summer of 2004, as many as 40.6% of the strains could be resistant
to both penicillin
(penicillin-resistant Streptococcus pneumoniae (PRSP)) and
erythromycin
(erythromycin-resistant Streptococcus pneumoniae (ERSP))
from just 8.6% in 1996; cefotaxime
for meningitis
.
It is produced by species in Lancefield groups A, C and G. Toxic even for
myocardiocytes and WBCs. It allows Streptococcus pyogenes NAD-glycohydrolase
(SPN) to enter host keratinocytes..
SPE-A is also complexed with hyaluronic acid and induces a type IV hypersensitivity
reaction at the second challenge, causing skin lesions typical of scarlet
fever. Titre of neutralizing Abs after exposure to a first challenge (i.e.
susceptibility
to scarlet fever) can be evaluated by Dick test : after intracutaneous
injection of SPE-A, type IV hypersensitivity (local erythema) occurs only
in individuals with low titres of neutralizing Ig, susceptible to scarlet
fever at the next challenge. Diagnosis of scarlet fever is instead
acquired by Schultz-Charlton reaction : after intracutaneous injection
of anti-SPE-A antitoxin or scarlet fever convalescent serum is injected
into an area of the skin showing a bright red rash, a blanching of the
skin at the site of the injection occurs. Serum from scarlet fever patients
does not produce this reaction.
converts plasminogen to plasmin [also used in therapy to clear blocked
arteries in patients who have heart attacks]
destroys capsule of Lancefield C and G serotypes.
protease
: pharyngitis
and tonsillitis, with an erythematous rash produced by an erythrogenic
toxin elaborated by the streptococci, progressing from the trunk and neck
to the arms, legs, forehead, and face, with flushed face and circumoral
pallor, white strawberry mucosa ===detersion==> red (hyperhemic)
strawberry tongue (enanthema), Rumpel-Leede phenomenon (the appearance
of minute subcutaneous hemorrhages below the area at which a tourniquet
is applied not too tightly for 10' upon the upper arm) and lines of skin
hyperpigmentation
(Pastia's sign) in the body creases; the rash disappears and is
followed by desquamation of the skin. Similar clinical manifestations,
but usually with involvement of the pharynx and tonsils, may follow infection
of wounds, burns, or the skin with group A b-hemolytic
streptococci, or with any strain of streptococci that elaborates an erythrogenic
toxin. Complications : otitis
media,
tonsillar
abscess, suppurative lymphadenitis,
mastoiditis,
sinusitis,
cerebral
abscess,
tubulointerstitial
nephritis.
Now usually milder than in the past when septic complications were common
after 6-7 days incubation
and necrotizing
fasciitis
(hence named "skin-eating streptococci" or "flesh eating Bacteria")
from M1 types (alone or in association with Staphylococcus
aureus). Several reports suggest that the incidence of invasive
GAS infections, including streptococcal toxic shock syndrome and necrotizing
fasciitis, is increasing. During 1992 and 1993 a prospective, population-based
surveillance of invasive group A streptococcal disease was conducted in
Ontario, Canada, where there is an annual incidence of 1.5 cases per 100
000 population. The rates were highest in young children and the elderly.
56% of the patients had underlying chronic illness. Risk factors for disease
included infection with the HIV, cancer, diabetes, alcohol abuse, and chickenpox.
The most common clinical presentations were soft-tissue infection (48%),
bacteremia with no septic focus (14%), and pneumonia (11%). Necrotizing
fasciitis occurred in 6% of patients, and toxic shock in 13%. The mortality
rate was 15% overall, but it was 29% among those over 64 years of age (P<0.001)
and 81% among those with toxic shock (P<0.001). 14% of the cases were
nosocomial, and 4% occurred in nursing home residents, often in association
with disease outbreaks. Invasive disease occurred in 2 household contacts
of patients with infection, for an estimated risk of 3.2 per 1000 household
contacts (95% confidence interval, 0.39 to 12 per 1000). The elderly and
those with underlying medical conditions are at greatest risk for invasive
GAS disease, toxic shock, and necrotizing fasciitis. Invasive steptococcal
infection is associated with a substantial risk of transmission in households
and health care institutions. Most cases occur outside of the hospital
setting. 2 patients were described with nosocomial streptococcal toxic
shock syndrome (StrepTSS). In patient 1, the syndrome was associated with
the development of necrotizing fasciitis following inguinal hernia repair.
Patient 2 suffered from StrepTSS shortly after receiving a tetanus vaccine
in her left deltoid. Epidemiologic investigations of these cases, which
were noted within 48 hours of each other, showed that the same surgeon
performed the vaccination on patient 2 after assisting a colleague during
the hernia repair procedure on patient 1. He was found to be a nasal carrier
of GAS. All GAS isolates from the patients and the surgeon were indistinguishable
by PFGE. PCR analysis demonstrated the presence of streptococcal pyogenic
exotoxins A and F. All strains !were of the T-1 serotype and possessed
the gene for M-protein 1. This report demonstrates that a virulent strain
of GAS may be spread by asymptomatically colonized medical personnel via
the air routeref.
An outbreak of infection due to Streptococcus pyogenes occurred
in a geriatric rehabilitation unit between Feb and Sep 1981, affecting
10 patients and 2 staff. The severity of the illness ranged from asymptomatic
throat carriage, through skin and soft-tissue sepsis, to fulminant septicemia
and necrotizing fasciitis: 2 patients died of their infection. Streptococcus
pyogenes infection may present in a variety of ways, and may be dangerous.
Recently developed serological tests have been found useful in the surveillance
of an outbreak. Although Streptococcus pyogenes is sensitive to
penicillin and other antibiotics, good ward hygiene is still essential
for controlling such an outbreak in an institutionref
on male genitals
/ streptococcal angina / strept throat (15% all pharyngitis)
after 2-4 days incubation : spots are smaller than in diphteria. Leukocytosis
with relative neutrophilia. Self-limiting within 5-7 days.
and DIC
; rarely necrotizing
fasciitis,
myositis
and gangrene.
by nephritogenous strains
from serotype M12 or M25.
almost always related to streptococcal pharyngotonsillitis
protease.,
sacroilitis, monoarthritis, endophthalmitis
and cranial nerve palsy are documented. Virtually all patients have been
farmers and butchers, of whom 80% were men. Most had been involved in butchering
sick pigs or selling the pork. > 40% of the patients were in the age group
50 to 60 years, and none were children.,
first reported in China in 1964, and is known locally as Xinjiang hemorrhagic
fever. Cases are reported from the south west region. 260 cases (54 fatal)
were reported in Xinjiang (southern desert region) during 1964 to 1995.
10 to 20% of sheep, goats, and cattle in Sichuan are seropositive. This
latter information raises the index of suspicion that CCHF is a likely
candidate. While CCHF is usually thought of as a tickborne disease, it
can also be transmitted through contact with infected bodily fluids from
people (in nosocomial outbreaks) and animals. Another of the hemorrhagic
fevers seen in the region is hemorrhagic renal syndrome associated with
hantavirus infection. The description above makes that diagnosis less likely,
although one must recognize that newswire descriptions may not necessarily
be representative of the actual clinical picture. Some of the features
of these illnesses are not characteristic of avian influenza; in particular,
the unrelatedness of the victims, the development of hemorrhagic symptoms
and shock, and the association with slaughter of pigs and sheep. The one
caution towards that being the diagnosis is the lack of mention of that
in the press articles, as one would expect that specimens have been sent
for testing of previously known hemorrhagic fever organisms. Virtually
all infection diseases begin with "flu-like" symptoms and this cannot be
taken as indicative of avian influenza virus infection. Furthermore the
role of pigs as a mixing vessel allowing interactions between human and
avian influenza viruses is an attractive hypothesis, but one that has still
to be substantiated. As of April, 23% of 450 Chinese pigs tested were carrying
a less virulent avian flu strain : H9N2. If it is
the case that the porcine streptococcus is the cause of these illnesses,
perhaps the organism has acquired one or more virulence factors (from,
for instance, the Group A streptococcus or Staphylococcus aureus)
to increase its transmissibility and virulence in humans. It would be interesting
to assess any medical co-morbidities in the infected cohort. The authorities
have dismissed speculation that the deaths were caused by bird flu, a virus
that has killed over 50 people in Asia since late 2003. Nevertheless, medical
experts outside mainland China said the unusually high mortality rate of
20% and reports that many of the 27 victims died within a day of showing
symptoms were inconsistent with what is known so far about human Streptococcus
suis infection.
(occupational disease expecially in breeders and slaughterers). The organism
is carried on the pig's tonsils and is spread pig-to-pig through nose rubbing
or coughing. But it's only found in small concentration on the pigs' tonsils,
so it's difficult for a human to catch it that way. When the infection
spreads to the brain, causing meningitis, it's in far greater concentration,
and so it can be transmitted to humans who eat raw infected pork or handle
the dead animal with open cuts. Although the governmental official states
that risk of infection is only present with open wounds, Kay's studyref
reported that only 20% of patients were noted to have sustained minor cuts
or burns before symptoms occurred. Finding that many patients had no history
of any injury, the authors speculate that respiratory or oral routes may
be important.
and streptococcal toxic shock-like syndrome (STSS / STSLS)ref
=> fulminant sepsis,
meningitis
followed by partial or permanent hearing loss),
endocarditis,
and a hemorrhagic diathesis can be associated with many bacteremic syndromes
after 6-7 days incubation
ref1,
ref2tisrefref1,
ref2,
ref3
(Loewe L, Rosenblatt P, Alture-Werber E. A refractory case of subacute
bacterial endocarditis due to Veillonella gazogenes clinically arrested
by a combination of penicillin, sodium paraaminohippurate, and heparin.
Am Heart J. 1946;32:327–38.) and from a lung abscess in a patient with
echocardiographic vegetations, but blood cultures were negativeref.
,
osteomyelitis,
prosthetic joint infection, pleuropulmonary infection, endocarditis,
and bacteremia. Veillonella spp. had also been isolated from intravenous
drug users with polymicrobial endocarditisref
has been the antimicrobial agent of choiceref.
However, recent studies found a notably high resistance to penicillin G
(MIC >= 2 mg/mL)ref.
These penicillin G–resistant isolates showed generally reduced susceptibility
to ampicillin or amoxicillin but remained susceptible to amoxicillin and
clavulanateref
and surgical infections that lead to clostridial
myonecrosis / gas gangrene
via toxinfections from anaerobically conserved vegetables and meats)
and Bos taurus)
and Bos taurus)),
herbivore mammals and home-caught and -prepared fish may occasionally contain
the organism as a transient.
neuroexocytosis by acting as :.
In the past a number of governmental military programs, including those
of the former Soviet Union, Nazi Germany, imperial Japan, and the US all
extensively weaponized the toxin. Indeed, even after the 1992 Biological
and Toxin Weapons Convention, the Soviet Union and Iraq allegedly continued
large-scale production of the toxin for offensive warfare purposes, and
the USSR was reported to have spliced the toxin gene into other bacterial
species
,
weak sucking ability and generalized weakness). In the USA, infant
botulism is the most common. Almost all known cases of the disease have
recovered : sometimes it causes sudden
infant death syndrome (SIDS).
Prompt treatment of infant botulism type A or type B with Human
Botulism Immune Globulin Intravenous (Human) (BIG-IV),
which neutralizes botulinum toxin, was safe and effective in shortening
the length and cost of the hospital stay and the severity of illnessref
for peptic ulcer diseaseref
or jejunoileal bypassref
or other functional intestinal disease, such as Crohn's
diseaseref
or a Meckel's
diverticulumref.
A 35 year old American woman living in Prague who traveled to the Republic
of Georgia for a week business trip developed colinzation botulism at return
in 2005 : even if acquired in Prague, a report of 4 cases thought to be
adult colonization botulismref
showed that toxin and/or C. botulinum can be found for prolonged
times in the stool, as long as 119 days. This is likely to occur with ingestion
of preformed toxin. In a murine model, lyophilized airborne botulinum spores
was found to be able to colonise antimicrobially pretreated adult miceref.
This observation may be relevant if a biowarfare situation when widespread
antimicrobials are utilized.,
palpebral
ptosis,
diplopia,
mydriasis
or anisocoria)
=> glossopharyngeal
(IX) nerve paralysis
and vagus (X) nerve
paralysis
(=> dysphagia
and dysarthria)
=> hypogloxal
(XII) nerve paralysis
and facial (VII) nerve
paralysis
=> xerostomia,
growing dim, dysphonia,
nausea
and vomiting,
diarrhea.
10-20% die within 24 hours due to bulbar paralysis, leading to respiratory
and heart failure. The duration of illness ranges from 1 day to several
months. The toxins also affect the adrenergic system but apparently with
insignificant consequences. Lethality = 30%.
contamination from serotypes A or B : 4÷14 dd. incubation :
among injecting drug users (IDUs)ref1,
ref2,
ref3,
ref4,
ref5.
A multivalent toxoid evokes good protective antibody response but its use
is unjustified due to the infrequency of the disease : an experimental
vaccine exists for laboratory workers.
,
homogous
hyperimmune antiserum,
or
rMAbs
as soon as possible after exposure; preferably within minutes but beneficial
effects may be achieved within the first few hours. The first (or only)
patient in an outbreak has a 25% chance of death, whereas subsequent cases
which are diagnosed and treated more quickly, carry only a 4% risk.
(NEC) (a.k.a. hemorrhagic enterotoxemia) in babies
(CDAD), fever, and leukocytosis in individuals treated with broad-spectrum
antimicrobials (e.g.: clindamycin,
carbopenems,
3rd
generation cephalosporins)
that has caused reduction of antagonism by indigenous symbiotic microflora
=> colonization of the colon => bacteraemia
=> extra-intestinal abscesses. Death may occurs by septic
shock,
hypovolemic
shock,
toxic
megacolon
and colonic perforation => peritonitis
,
vancomycin,
teicoplanin,
or fusidic acid
is usually effective, but, relapse may occur. Saccharomyces boulardiior
Saccharomyces
cerevisiae.
and surgical infections that lead to clostridial
myonecrosis / gas gangrene
and surgical infections that lead to clostridial
myonecrosis / gas gangrene
and surgical infections that lead to clostridial
myonecrosis / gas gangrene
and surgical infections that lead to clostridial
myonecrosis / gas gangrene
than staphylococcal enterotoxin B disease,
minimal if any nausea and
vomiting,
usually no fever. Resembles emetic form of Bacillus
cereus food poisoning.
ileal overgrowth causes equine dysautonomia / equine grass sickness
(EGS) / "mal seco" : acute, subacute, or chronic widespread autonomic
nervous system (ANS) dysfunction
(NEC) (a.k.a. hemorrhagic enterotoxemia) in babies and adults
when trypsin-mediated degradation of b toxin
is impaired :
.
looking for b toxin.
.
.
and
surgical infections that lead to clostridial
myonecrosis / gas gangrene
,
citing 2 more deaths after its use. At least 5 women in the USA have died
after taking the pill since it began selling in 2000, although the FDA
stressed that it could not prove the drug was to blame. The 4 deaths caused
by sepsis,
all occurred in women who didn't follow FDA-approved instructions for a
pill-triggered abortion : 2 of these deaths occurred in 2003, 1 in 2004,
and 1 in 2005. The action comes just 8 months after the FDA warned about
2 sepsis cases associated with Mifeprex. Additional sepsis cases were reported
to the agency in April and June 2005. The drug, sold by Danco Laboratories,
NY, is approved to terminate pregnancy up to 49 days after the beginning
of the last menstrual cycle : when followed by misoprostol the pregnancy
is terminated. The FDA's instructions call for women to swallow both pills,
but most abortion clinics instead instruct that the misoprostol tablet
be inserted into the vagina. Studies have shown it can work that way, too.
But the 4 sepsis deaths, all reported from California, came after this
so-called off-label use. Officials couldn't say whether the women had inserted
the tablet vaginally themselves. In 2 of the infections, doctors identified
Clostridium
sordellii, a common germ not usually associated with illness. The other
USA death associated with Mifeprex was a case of a ruptured ectopic, or
tubal, pregnancy in October 2001. The drug is not to be used by women with
suspected or confirmed ectopic pregnancies, a life-threatening condition
in which the fertilized egg has implanted outside the uterus. The FDA is
investigating recently reported serious adverse events associated with
mifepristone. As a result, the FDA is issuing public health advice Tue
19 Jul 2005 highlighting the risk of sepsis, or blood infection, when undergoing
medical abortion using Mifeprex and misoprostol in a manner that is not
consistent with the approved labeling. There are now 4 cases of deaths
from infection from September 2003 to June 2005 following medical abortion
with these drugs. Mifeprex was approved by the FDA in September 2000, mifepristone
is a safe and effective drug that offers women a non-surgical option for
regnancy termination, an option that many women feel affords them greater
privacy and autonomy. Mifepristone, like every drug, presents a certain
degree of risk. However, that risk should be considered in the context
of the broader risk of maternal mortality. Serious and sometimes fatal
infections occur very rarely following miscarriage and surgical and medical
abortions, and the risk of infection following medical abortion remains
very low. A few statistics: In the USA, reports of all infections following
Mifeprex are < 1%. To put the safety of medical abortion in perspective,
there are about 13 pregnancy-related deaths per 100 000 live births. Abortion,
whether medical or surgical, is much safer than pregnancy and childbirth.
Furthermore, it should be understood that the "off label" use of mifepristone
itself does not present a risk to women who use the drug. Evidence-based
regimens of mifepristone medical abortion are widely used in the USA and
abroad, which reduce rather than increase a woman's risk of serious side
effects. The challenge now for health care professionals, patient advocates,
and health journalists will be to communicate accurate and clear information
about these methods so women who are considering the option of abortion
can make informed decisionsref1,
ref2.
For more information about the revised mifepristone labeling, see here.
In addition, a fatal case of C. sordellii toxic shock syndrome after
medical abortion with mifepristone and misoprostol was reported in 2001,
in Canada (2). All 3 cases of C. sordellii infection were notable
for lack of fever, and all had refractory hypotension, multiple effusions,
hemoconcentration, and a profound leukocytosis. C. sordellii previously
has been described as a cause of pregnancy-associated toxic shock syndrome
(3).
ref,
and neonatal omphalitis (infection of the umbilical stump)ref.
In addition, the organism has been associated with contaminated musculoskeletal
tissue allograftsref
in 2001 and 2002. Fatal postpartum infection with C. sordellii,
spontaneous endometritisref1,
ref2,
ref3,
and fatal C. sordellii infection associated with medical abortion
have all been reportedref.
These cases tend to be fulminant toxic shock-like illnesses associated
with a markedly elevated WBC count and massive capillary leak with loss
of plasma from the intravascular spaceref.
It appears that vaginal colonization with Clostridium spp. increases
during pregnancy, and the overwhelming toxemia is a manifestation of ascending
infection to the inner lining of an area (the pregnant (or peripregnant)
uterus able to absorb the toxinref
and surgical infections that lead to clostridial
myonecrosis / gas gangrene.
,
pleuropulmonary infection
and GABA
release => hyperexcitability of the downstream motoneurons => spastic
paralysis. The toxin is O2- and protease-labile (destroyed
by gastric juice) and and can be destroyed at 65°C in 5'. LD50
: 500 pg/kg (= 40 pg in Mus
musculus, 130 mg in humans) The toxin
can't cross the blood-brain barrier.
(such as from a metal nail, wood splinter, or insect bite)
(differential feature from rabies)
=> respiratory spasm => death.
and systemic
arterial hypertension
("vascular dance"). Fever
is the differential symptom from strychnine
poisoning.
Complications : bronchopneumonia,
pulmonary embolism, urinary
tract infections (UTI)
due to bladder paralysis, sepsis,
constipation,
bone
fractures
due to paroxysmal spasms.
,
curarization, positive pressure respiration, heterologous
or homologous
hyperimmune antiserum,
avoid sensorial afferences that could trigger reflex arches.
(in association with Streptococcus spp.
and Enterobacteriaceae)
and lung abscess
.
and Strigops
habroptilus).
A
variety of mammals are also affected, with Sus
scrofa
being the most economically important species. Infection in reptiles
and amphibians has also been reported. The organism has been isolated from
the surface slime on fish, which may serve as a source of infection for
other species. It can survive in soil for 35 days under a variety of conditions.
Humans usually become infected when the organism enters through cuts in
the skin, most common in people who handle infected tissues, such as veterinarians,
butchers, and fish handlers.
(fever),
endocarditis
of aortic valve, or, septic
arthritis,
among other manifestations, and resolves spontaneously within 2-3 weeks
or is sometimes fatal,
or erythromycin,
but is resistant to vancomycin.
As soon as a presumptive diagnosis is made, penicillin should be administered
IM at 10 000 u/lb body wt simultaneously with a full dose of erysipelas
bacterin. Experimentally, the incubation period can range from 44 hrs to
several weeks
(?)
with chills, malaise, dry cough,
headache,
pharyngitis,
otitis
media,
myocarditis,
pericarditis,
tracheobronchitis, erythema. Self-limiting within 8 weeks, lethality <
1% Polished-glass lung look at Rx. Complications : type II hypersensitivity
(a frigore Igs against I Ag on RBCs) leading to hemolytic
anemia.
,
erythromycin.
Resistant to penicillins
and Tl acetate (used in selective culture media). Antiserum ; killed
or attenuated
vaccine.
: usually it is released in the medium during the post-logarithmic phase
of growth or after bacterial cell lysis (only Pseudomonas
aeuruginosa and Neisseria meningitidis
release it by blebs)
(sometimes TLR2)
and induces synthesis of COX-2, IL-1b,
IL-2,
IL-6,
CXCL8
/ IL-8,
IL-10,
IL-12,
IL-18,
IFN-g,
TGF-b1
and TNF-a,
that in turn cause :
(LPS was once named exogenous pyrogen)
synthesis in hepatocytes => great ESR
increase,
decrease in heart contraction and increase in resistance of pulmonary blood
vessels => systemic
arterial hypotension
=> septic shock,
producing autoimmune reactions.,
LDL
and LPS-binding
protein (LBP):
in the latter case LPS-LBP complex may bind CD14.
When injected twice, it produces the Shwartzman reaction :
,
widespread hemorrhages, and a marked fall in leukocyte and platelet counts
and usually results in death of the animal,
which leads to a decrease in serum killing, allowing a certain threshold
of bacteraemia
and intrabdominal and lung
abscesses
in
babies
,
ampicillin/sulbactam,
piperacillin-tazobactam,
or meropenem
bite wounds,gingivitis
protease
,
gingivitis,
noma
/ cancrum oris / gangrenous stomatitis,
adult
periodontitis
and lung abscess
,
gingivitis
protease
bites
(25%), septicemia, meningitis,
endocarditis,
and rare ocular infectionsref1,
ref2
bites
=> septicemia(in
immunocompromised hosts) => DIC,
endocarditis,
alveolar
pneumonia,
symmetric
peripheral gangrene, cellulitis,
acute
pyogenic suppurative thyroiditis,
lymphadenitis,
osteomyelitis
=> septicemia
(in immunocompromised hosts) => DIC,
endocarditis,
alveolar
pneumonia,
symmetric
peripheral gangrene, cellulitis,
acute
pyogenic suppurative thyroiditis,
lymphadenitis,
osteomyelitis
=> septicemia
(in immunocompromised hosts) => DIC,
endocarditis,
alveolar
pneumonia,
symmetric
peripheral gangrene, cellulitis,
acute
pyogenic suppurative thyroiditis,
lymphadenitis,
osteomyelitis