Humans are the primary reservoir for the HSV-1 virus
CCHFV reservoir is ticks, while the HSV1 reservoir is humans.
Humans are the primary reservoir for the HSV-1 virus
CCHFV reservoir is ticks, while the HSV1 reservoir is humans.
The prevalence is highest in Africa (87%)
Both CCHFV and HSV1 have the highest prevalence in Africa.
Specific species of ticks (such as those in the Hyalomma genus) represent the reservoir of the virus
CCHFV reservoir is ticks, while the HSV1 reservoir is humans.
Crimean-Congo Hemorrhagic Fever Virus (CCHFV) commonly infects people throughout Africa
Both CCHFV and HSV1 have the highest prevalence in Africa.
M. tuberculosis, acquired drug resistance is caused mainly by spontaneous mutations in chromosomal genes, producing the selection of resistant strains during sub-optimal drug therapy
acquired resistance
P. mirabilis produces mannose-resistant Proteus-like (MR/P) pili, which are CUP pili that facilitate biofilm formation and colonization of the bladder and kidneys, and are crucial for catheter-associated biofilm formation
virulence
Enterococcus 2%
prevalence
Treatment for Uncomplicated UTIs UTIs in low-risk women can often be successfully treated over the phone. In such cases, a health professional provides the patients with 3-day antibiotic regimens without requiring an office urine test. This course is recommended only for women at low risk for recurrent infection, who do not have symptoms (such as vaginitis) suggesting other problems. Antibiotic Regimen . Oral antibiotic treatment cures 94% of uncomplicated urinary tract infections, although the rate of recurrence remains high. The following antibiotics are commonly used for uncomplicated UTIs: The standard regimen has traditionally been a 3-day course of trimethoprim-sulfamethoxazole, commonly called TMP-SMX (Bactrim, Cotrim, Septra). TMP-SMX combines an antibiotic with a sulfa drug. A single dose of TMP-SMX is sometimes prescribed in mild cases, but cure rates are generally lower than with 3-day regimens. Allergies to sulfa are common and may be serious. Fluoroquinolone antibiotics, also called quinolones, have usually been a second choice. However, in geographic areas that have a high resistance to TMP-SMX, quinolones are now the first-line treatment for UTIs. Ciprofloxacin (Cipro) is the quinolone antibiotic most commonly prescribed. Quinolones are usually given over a 3-day period. Pregnant women should not take these drugs. Nitrofurantoin (Furadantin, Macrodantin) is a third option. This drug must be given for longer than 3 days. Fosfomycin (Monurol) is not as effective as other antibiotics but may be used during pregnancy. Resistance rates to this drug are very low. Other antibiotics may also be used, including amoxicillin (with or without clavulanate) and cephalosporins. Doxycycline is often effective but cannot be given to children or pregnant women.
treatment
Symptoms of lower urinary tract infections usually begin suddenly and may include one or more of the following signs:
symptoms
Vesicoureteral Reflux (VUR). Vesicoureteral reflux (VUR) affects about 10% of all children and is the cause of up to 50% of urinary tract infections during childhood.
children risk factor
Benign prostatic hyperplasia (BPH), enlargement of the prostate gland, can produce obstruction in the urinary tract and increase the risk for infection.
male risk factor
Specific Risk Factors in Women
risk factors
Escherichia (E.) coli is responsible for most uncomplicated cystitis cases in women, especially in younger women. E. coli is generally a harmless microorganism originating in the intestines. If it spreads to the vaginal opening, it may invade and colonize the bladder, causing an infection. The spread of E. coli to the vaginal opening most commonly occurs when women or girls wipe themselves from back to front after urinating, or after sexual activity. Staphylococcus saprophyticus accounts for 5 - 15% of UTIs, mostly in younger women. Klebsiella , Enterococci bacteria, and Proteus mirabilis account for most of remaining bacterial organisms that cause UTIs. They are generally found in UTIs in older women. Rare bacterial causes of UTIs include ureaplasma urealyticum and Mycoplasma hominis , which are generally harmless organisms. Organisms in Severe or Complicated Infections The bacteria that cause kidney infections ( pyelonephritis ) are generally the same bacteria that cause cystitis. There is some evidence, however, the E. coli strains in pyelonephritis are more virulent (able to spread and cause illness). Complicated UTIs that are related to physical or structural conditions are apt to be caused by a wider range of organism. E. coli is still the most common organism, but others include Klebsiella , P. mirabilis , and Citrobacter . Fungal organisms, such as Candida specie s. ( Candida albicans causes the "yeast infections" that also occur in the mouth, digestive tract, and vagina.) Other bacteria associated with complicated or severe infection include Pseudomonas aeruginosa , Enterobacter, and Serratia species, gram-positive organisms (including Enterococcus species), and S. saprophyticus .
bacterial causes
About 25 - 50% of these women can expect another infection within a year of the previous one. Between 3 - 5% of women have ongoing, recurrent urinary tract infections, which follow the resolution of a previous treated or untreated episode.
prevalence of recurrence
Recurrences occur in up to 50 - 60% of patients with complicated UTI if the underlying structural or anatomical abnormalities are not corrected.
recurrence
95% of cases of UTIs are caused by bacteria that typically multiply at the opening of the urethra and travel up to the bladder. Much less often, bacteria spread to the kidney from the bloodstream
cases
UTIs are the most common of all bacterial infections and can occur at any time in the life of an individual.
prevalence
Drug Resistant TB Is Predicted To Steadily Spread In 4 Countries
Pathogens in the News Article
only case of keratitis
These 24 isolates had the following profiles of resistance against 16 antibiotics: all the isolates were resistant to cephalothin and vancomycin and 95.8% were resistant to ampicillin.
antibiotic resistance
For molecular biology experiments, S. putrefaciens strains were grown aerobically at room temperature (23 to 25°C) or at 30°C on Luria-Bertani (LB) medium, pH 7.4 (42)
growth conditions
Growth ConditionsTemperature: 30.0°CAtmosphere: Aerobic
growth conditions
β-lactams inhibit bacterial cell wall synthesis by binding to one or more of the penicillin-binding proteins (PBPs). This inhibits the final transpeptidation step of peptidoglycan synthesis in bacterial cell walls, thus inhibiting cell wall biosynthesis. Bacteria eventually lyse due to ongoing activity of cell wall autolytic enzymes (autolysins and murein hydrolases) in the absence of cell wall assembly.[9] Due to the mechanism of their attack on bacterial cell wall synthesis, β-lactams are considered to be bactericidal.
mechanism of action
β-lactam antibiotic
mechanism of action
most Shewanella infections are treated easily by a combination of surgical therapy/drainage and antibiotics
treatment
S. putrefaciensT (ATCC 8071)
test results
all S. alga strains produced a hemolytic reaction on sheep blood agar while S. putrefaciens isolates lacked this activity.
no hemolysis for S. putrefaciens
implicated occasionally as a human pathogen, it is most frequently recovered from nonhuman sources, including aquatic reservoirs (marine, freshwater, and sewage), natural energy reserves (oil and gas), soil, and fish, poultry, dairy, and beef products
reservoirs
Transmission route for 183 (52%) was foodborne, 74 (21%) unknown, 50 (14%) person-to-person, 31 (9%) waterborne, 11 (3%) animal contact, and 1 (0.3%) laboratory-related
outbreak
Although Tir is essential for the strong bacterial attachment to host cells, and is a key molecule involved in the attaching and effacing lesion observed during infection, it has since been discovered to suppress innate immune signaling pathways
immune evasion
extracellular pathogens such as members of the Attaching and Effacing (A/E) pathogen group that include enteropathogenic E. coli (EPEC), enterohemorrhagic E. coli O157:H7 (EHEC), and Citrobacter rodentium, inhibit innate immune responses while maintaining intimate contact with the host plasma membrane
immune evasion
A second cardinal virulence factor of E. coli O157:H7 is Shiga toxin, which causes bloody diarrhea and hemolytic uremic syndrome (HUS), a sequelae of EHEC infection. E. coli O157:H7 produces Stx-2, an A-B toxin comprised of a single A subunit noncovalently associated with a pentamer of B subunits. The B subunits bind specifically to globotrioacyl ceramide on host cell cytosolic membranes and facilitates A-subunit uptake by endocytosis. Stx is an N-glycosidase that targets the 28S rRNA, which it depurinates at a specific adenine residue, causing protein synthesis to cease and infected cells to die from apoptosis
virulence
Lipid A is the toxic component of LPS, also known as endotoxin, which is a heat-stable toxin
virulence
outer facing leaflet of lipopolysaccharide (LPS)
virulence
Locus of Enterocyte Effacement (LEE), which is contained on a pathogenicity island that encodes all of the gene products needed for attaching and effacing the colonic epithelium
virulence
Sorbitol non-fermenting colonies should be assayed for Shiga toxin using EIA or PCR
lab tests
cefixime tellurite-sorbitol MacConkey agar (CT-SMAC), or CHROMagar O157
culturing
four distinct systems for acid tolerance. There are four corresponding acid resistance (AR) gene systems. The mechanism of AR1 is unknown. AR2, AR3, and AR4 each depend upon amino acid decarboxylation and consequent consumption of protons, whcih results in pH homeostasis. Expression of the AR systems is induced by acid environment, anaerobiosis, entry into stationary phase. Collectively, one or more of these systems is likely to be "on" when EHEC is exposed to acid, as would be expected to occur upon consumption by a potential host and subsequent passage through the stomach
virulence
EHEC virulence factors include the ability to adhere tightly to plant materials, acid tolerance, attachment and effacement of intestinal epithelium, and production of endotoxin and Shiga toxin. The regulator of "hyper-adherence", TdcR, and OmpA, an outer membrane protein that is expressed during hyper-adherence are implicated in binding of EHEC to alfalfa sprouts and seed coats. Loss of these virulence factors results in decreased adherence.
virulence
E. coli O157:H7 readily colonizes the mammalian large intestine, including humans
colonization
Tissue tropism of EHEC at the rectal-anal junction and its stable colonization at this anatomical location ensures its persistence and shedding in feces
colonization
Treatment of EHEC typically involves rehydration without administration of antibiotics and hospitalization in severe cases, especially HUS.
treatment
E. coli pathotypes that cause diarrhea are transmitted via contaminated food or water, or through contact with infected animals or people
spread of infection
motile by means of peritrichous flagella
motility
facultative anaerobe
O2
Gram negative rod
gram neg, shape
E. coli (EHEC) typically cause acute bloody diarrhea, which may lead to hemolytic-uremic syndrome. Symptoms are abdominal cramps and diarrhea that may be grossly bloody. Fever is not prominent.
symptoms
Multistate Outbreak of Shiga toxin-producing Escherichia coli O157:H7 Infections Linked to I.M. Healthy Brand SoyNut Butter (Final Update)
outbreak
Bovine manure can harbor viable EHEC for more than seven weeks (Wang et al., 1996), and the long-term environmental persistence of EHEC poses an increased risk for transmission of EHEC through the fecal-oral route through wash-off to nearby farms or in contaminated grass consumed by other cattle.
public health concern
humans acquire EHEC by consuming contaminated bovine-derived products such as meat, milk, and dairy products (Armstrong et al., 1996) or contaminated water, unpasteurized apple drinks, and vegetables (Cody et al., 1999; Hilborn et al., 1999; Olsen et al., 2002). Direct contact with ruminants at petting zoos or through interactions with infected people within families, daycare centers, and healthcare institutes represent another source of EHEC transmission
transmission
EHEC colonizes in the colon and causes electrolyte imbalances
virulence
Antibiotics promote Shiga toxin production by enhancing the replication and expression of stx genes that are encoded within a chromosomally integrated lambdoid prophage genome. Stx induction also promotes phage-mediated lysis of the EHEC cell envelope, allowing for the release and dissemination of Shiga toxin into the environment
Antibiotics --> increased Shiga toxin production
patients treated with antibiotics for EHEC enteritis had a higher risk of developing HUS
Antibiotics complications
Currently no treatment is available for EHEC infections (Goldwater and Bettelheim, 2012). The use of conventional antibiotics exacerbates Shiga toxin-mediated cytotoxicity
Antibiotics contraindicated
life-threatening complication hemolytic uremic syndrome (HUS)
complication
Cattle are a natural reservoir of EHEC, and approximately 75% of EHEC outbreaks are linked to the consumption of contaminated bovine-derived products
reservoir
antimicrobials trigger an SOS response in EHEC that promotes the release of the potent Shiga toxin that is responsible for much of the morbidity and mortality associated with EHEC infection
virulence factor
Enterohemorrhagic Escherichia coli (EHEC) serotype O157:H7 is a human pathogen responsible for outbreaks of bloody diarrhea and hemolytic uremic syndrome (HUS) worldwide
EHEC --> bloody diarrhea
Previously healthy and no risk factors for drug-resistantS. pneumoniae(DRSP) infection:A. A macrolide (azithromycin, clarithromycin, orerythromycin) (strong recommendation; level Ievidence)
Treatment
commercially available radioimmunoassay for bacterial antigen in urine is satisfactory, but is available only for serogroup 1 of L pneumophila
possible test
possesses pili (fimbriae), and most species are motile by means of a single polar flagellum
examination of bacteria
rate of invasive disease is about 10 cases out of every 100,000 non-pregnant adults
Prevalence of GBS
Most cases of group B strep disease in adults are among those who have other medical conditions that put them at increased risk, such as:
GBS in immunocompromised individuals
Group B strep disease is usually treated with penicillin or other common antibiotics
GAB treatment = penicillin
normal residents of the vaginal flora in 25% of healthy women
GBS presence in women
Clinical manifestations of adult GBS infection are varied and include skin, soft tissue and urinary tract infections, bacteremia, pneumonia, arthritis and endocarditis
GBS diseases
invasion of host cell barriers such as the epithelial and endothelial cells
GAB attachment
Group B Streptococcus (GBS) are generally beta hemolytic on blood agar plates (right hand side)
GBS - beta-hemolytic
Bacteria under Microscope Streptococcus agalactiae Group B streptococcus, GBS
GBS microscopy/streak plate photos
thoseharboringgroupBweremorelikelytohaveenlargedtonsils(P<0.001),exudate(P<0.02),andtenderenlargedanteriorcervicallymphnodes(P<0.01)
GBS signs and symptoms
DetectionofGBScanbe determined directly from broth media using latex agglutination, probes or nucleic acid amplification tests (NAAT) such as PCR
GAB tests
Procedures for processing clinical specimens for culture of group B Streptococcus (GBS) (s
Growth of GAB
Asymptomatic carriage in gastrointestinal and genital tracts is common. Intrapartum transmission via ascending spread from the vagina occurs. Mode of transmission of disease in non-pregnant adults is unknown.
GBS transmission/host
S. pneumoniae cultures are α-hemolytic on blood agar medium
Alpha hemolysis of GAB
Gram-Positive, Catalase-Negative Genera
GBS (Strep Pneumo.) = gram + and calalase -
A clearing of the turbidity in the bile tube but not in the saline control tube indicates a positive test, i.e., the pneumococcal cells have lysed ("solubilized").
Bile esculin test
Resistance of Group B Streptococcus to Selected Antibiotics, Including Erythromycin and Clindamycin
GAB resistance
TABLE III. MicrobiologyAerobicGram-positive cocciStaphylococcus aureus27MRSA3Coagulase-negative Staphylococcus40 (incl S epidermidis, S hemolyticus)StreptococcusBeta-hemolytic70Group A40Group B17 (incl S agalactiae, 1)Group D6 (non-Enterococcus)Group F5Group G2Alpha-hemolytic/S viridans31
Table of prevalence of S. aureus, Group A strep, Group B strep, and S. viridans
vancomycin creep
Potential that "vancomycin creep" is method dependent
S. aureus, there are only a handful of vancomycin-resistant strains
Vancomycin resistance found in S. aureus
methicillin-resistant Staphylococcus aureus (MRSA), methicillin-resistant Staphylococcus epidermidis (MRSE) and amoxicillin-resistant enterococci
Main uses of Vancomycin = bacterias with resistance to other antibiotics, perhaps not usual first line of defense if organism isn't known
many side effects including vestibular and renal, most likely due to impurities
Early side effects often correlated with impurities as opposed to antibiotic itself
Some resistance to er ythromycin, the agentof choice for penicillin-allergic patients with streptococ-cal phar yngitis, has been reported
Antibiotic resistance
High-dose penicillin G remains the antibiotic ofchoice for treatment of GAS, with no resistancerecorded.
Antibiotic of choice
Proteinases and other enzymes might con-tribute to tissue destruction
Virulence factor - tissue destruction
Streptococcal toxic shock syndrome (STSS) canbe associated with invasive infections secondar y toGAS infection
Virulence factor - toxicity
GAS grows best on complex “rich” medium such as Trypticase Soy Agar (TSA) supplemented with 5% Sheep Blood
Ideal growth
S. pyogenes is a facultative anaerobe and is grown at 37°C in either ambient air or in 5–10% CO2
Growth conditions
thoroughly cleaned and debrided
Was wound cleaned after bite/scratch?
Animals do not have to be ill to pass the bacterium to humans, as they can carry the organism without showing symptoms.
Has pt been bitten or scratched by an animal, even if animal has not appeared ill?
develop into a serious soft tissue infection, and can also be complicated by abscesses, septic arthritis and osteomyelitis. Pasteurella spp can also cause meningitis, ocular infections, and respiratory infections, usually in patients with underlying pulmonary disease.
What are the pt's signs and symptoms? Obvious skin differences near location of bite/scratch? Difficulty moving near injury? Neck pain? Difficulty breathing?
P. multocida is found worldwide
Location of pt and/or animal may not be telling for a pasteurella infection
caused by infection with bacteria of the Pasteurella genus
Bacterial infection - consider types of antibiotics that would be effective
zoonotic disease
Contracted from animals
"Were you bitten or scratched by an animal recently?"
respiratory tract and cause sinusitis and ear infections, and more severe symptoms including pneumonia or lung abscesses in those with underlying pulmonary disease, however this is rare. Other uncommon presentations of P. multocida infection include septicaemia (blood poisoning), eye infections, meningitis and gastrointestinal problems
Serious complications spread to signs and symptoms in the respiratory tract, blood, meninges, etc.
Exposure to aerosols, bites or scratches involving animals or injuries from objects contaminated with body fluids from animals require immediate first aid and medical attention
Less likely, but infection can also occur from contact with infected animal bodily fluid, such as contact with infected object
seek medical attention as soon as possible
How long ago did the injury/infection occur?
abscesses, cellulitis (an area of spreading inflammation) and joint infections
Most common complications stay near the site of infection
abscesses, cellulitis (an area of spreading inflammation) and joint infections
What does the wound look like in the pt?
local wound infection
Typical presentation
persons with a weakened immune system are at higher risk
Does the pt have a weakened immune symptom?