Gram positive stain

Epidemiology

Disease: Signs and Symptoms

Southeast Asia

encephalitis

Humans are the primary reservoir for the HSV-1 virus

The prevalence is highest in Africa (87%)

Introduction

Immunocompromised people are at risk of getting keratitis or encephalitis

Specific species of ticks (such as those in the Hyalomma genus) represent the reservoir of the virus

Crimean-Congo Hemorrhagic Fever Virus (CCHFV) commonly infects people throughout Africa

Mechanism of Viral Protein Synthesis and Replication

Vaccination, Treatment & Public Health Concerns

The sepsis rate was 1.81 per 1000 pregnant women. Escherichia coli was the predominant pathogen, followed by Group B Streptococcus.

parotid glands

encephalitis (2). If the virus is able to infect the cerebrospinal fluid, it travels within the ventricles where the CSF is produced (2). The virus then replicates within these areas and can penetrate into the brain and destroy some of the epithelial integrity, causing it to disintegrate into the CSF (2).

HPV infection has been known to progress to cancer

an injury to the epithelium allows the virus a portal of entry

The target of the virus is the stem cell, or the cells that are dividing (3). When the epithelial membrane is disturbed through damage or microabrasions, the virus is able to invade and infect the basal membrane where the dividing cells are located

HPV enters the host cell either through clathrin-mediated endocytic pathways

HCV causes mortality in the form of hepatitis and liver cancer

As such, the portal of exit comes in the form of puncturing the blood vessels and transferring viral particles from the blood of the victim to someone else

Rarely, through infected blood In theory, the virus could be spread through a blood transfusion.  To date, there are no known reports of this happening.

South East Asia

encephalitis

spreads through the air

synthesize a positive-strand antigenome,

97% effective vaccine MMR

Currently, there are no existing vaccinations against Epstein-Barr virus.

Human Parainfluenza virus (HPIV) is associated with causing lower respiratory diseases.

There are two mosquito species linked to most outbreaks of Zika, A. aegypti and A. albopictus.(1)

t.3 Interestingly, though eukaryotic mRNA has a 3’ poly(A) tail, flaviviruses lack this trait.4

Spread by mosquitoes

Like other flaviviruses, the yellow fever virus lacks a poly A tail.

Global Public

receptor-mediated endocytosis

Most of the influenza viruses that are dangerous to humans are found in horses and pigs, along with many avian species4. Many of the common influenza reservoirs that carry human infectious subtypes are either humans or birds4. There have also been cases of pigs being reservoirs for human infectious influenza,

Ebola

fever,

The Lassa virus genome contains two single-stranded RNA segments, one large one that is responsible for encoding the viral polymerase and zinc binding proteins and a smaller one that encodes the structural proteins.

fever

RSV is a medium-sized (120-200nm) enveloped virus with a negative-sense, single-stranded RNA genome

releases its negative RNA into the cytoplasm, RSV replicase begins base pairing to form the positive RNA template strand

after it enters the body through a mucous membrane, like the eye or nos

SV is often considered a nosocomial infection due to its prevalence in hospital settings, ranging from 6-56% from neonatal/pediatric to adult settings

human contact from the spread of infected respiratory secretions like mucous

human-human contact

The first step is to transcribe a positive sense RNA strand from the original negative sense RNA strand

Ebola enters the human host via mucosal areas or skin abrasions.

The primary reservoir of Ebola is thought to be fruit bats. It is not fully understood how Ebola jumped species.

Lastly, health-care providers who treat Ebola-infected patients are at high risk of contamination, as infections have occurred in the past when precautions were not strictly enforced

bola originally jumped to the human species from close contact with fruit bats, their excretions, or their blood (5). After that, transmission is through human-human contact, more specifically through direct contact with bodily fluids and/or anything carrying these fluids

Genomic Replication Cycle

(NS1, NS2A, NS2B, NS3, NS4A, NS4B, NS5) are involved in the construction of the replication complex which is key to successful RNA replication

single stranded RNA that is positively charged

Part 3: Zika Replication

receptor-mediated endocytosis begins

positive-sense single stranded RNA

Internalized

Positive-sense RNA strand ((+)RNA)

translated protein gets cleaved by virally encoded proteases and then yields

Positive sense, single-stranded-RNA (ssRNA) (8)

joint pain,

n regards to how this virus is transmitted, it is done by getting bitten by the female Aedes aegypti mosquito, which drank blood from an individual infected with the flavivirus, thus becoming infected itself (2)

joint pain

mosquito vector bites an infected viral reservoir

initiate entry into the host cell via receptor mediated endocytosis

attaching to epithelial cells in the lumen of the small intestine, which are non-dividing, mature enterocytes near the tips of the villi.

human monoclonal antibodies that target Nipah G glycoprotein

To date, there are no known vaccines.

typically fever and  a headache

Currently, there is no vaccine for the Marburg viru

tissue, body fluids, and secretions

The Marburg virus is zoonotic,

For the rabies virus, it's believed that replication takes place in protein aggregates within the cytoplasm called Negri bodies, which are more generally called cytoplasmic inclusion bodies

Exactly how the rabies virus enters the host cell is not yet clearly defined (2). The glycoprotein, which covers the surface of the virus and is involved in attachment, however, is also involved in entry into the cell (2). Before entering the cell, the virus enters a clathrin-coated pit on the exterior of the cell and binds (Figure 4) (2). Fusion of the vesicle, which is the membrane surrounding the virus, to the host cell plasma membrane and internalization of the virus is triggered by a decrease in pH (2). It is also mediated by the glycoproteins of the rabies virus (2). These glycoproteins are necessary for membrane fusion to occur, although even if fusion is inhibited, inhibition can also be reversed (2). Once the virus has entered the cell it is uncoated, meaning it releases its viral genome into the cytoplasm (2). It is believed this either occurs right after internalization into a neuron (likely at the presynaptic or postsynaptic end) or at some point after the virus has been transported to the cell body of the neuron (2).

Rabies virus is a zoonotic disease, meaning it can be spread between humans and other animals (1). It's often spread through animal bites

The poxviruses are unique compared to other DNA viruses in that they replicate their genome in the cytoplasm

There has been no evidence of person-to-person transmission

Treatment

Mechanism of Viral Replication

genome

zoonotic transmission

including the common cold, bronchitis, pneumonia,

These integrin proteins signal to the cell to endocytose the cell (receptor-mediated endocytosis), which engulfs the adenovirus in a clathrin-coated vesicle

negative-sense, single-stranded RNA genome

ticks infected with CCHFV

which progresses to a severe respiratory disease

The hantavirus virion first attaches to its target cell, pulmonary endothelial cells, by using the protein αVβ3 integrin as a receptor (Borges). Next, the virion enters the targeted cell via endocytosis (Vaheri).

VZV is transmitted through respiratory droplets, direct and indirect contact.

probably involves either endocytosis

being neurotropic

cell surface

symptomatically

luctuating climates

recently

transmission

The initial symptoms o

Enterovirus genus

categorized alongside poliovirus

ers into the cell's cytosol.

RME

Caroline Beuligmann

The viral envelope of the Marburg virus includes glycoproteins (GP) that acts as a ligand and interact, by binding or sending signals, with cellular molecules on the host cell surface (Takada).

Current findings suggest that almost anyone is a susceptible host for Marburg virus (Martines).

a (See Figure 1 and Table 2)

released via budding.

hree proteins—P, V, and C.

Life cycle of the measles virus

lipid rafts

peplomers

see figure 1

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

Otitis media and acute bronchitis due to H. influenzae are generally caused by nontypeable strains. Hib strains account for only 5%–10% of H. influenzae causing otitis media.

The other anaerobes tested – A. vaginae, M. mulieris, P. bivia, Veillonella, Peptostreptococcus and Peptoniphilus – demonstrated significantly lower biofilm formation relative to G. vaginalis (Student's t-test, P<0.0001).

Analysis of adherence, biofilm formation and cytotoxicity suggests a greater virulence potential of Gardnerella vaginalis relative to other bacterial-vaginosis-associated anaerobes

Many mycoplasmal pathogens exhibit filamentous or flask-shaped appearances and display prominent and specialized polar tip organelles that mediate attachment to host target cells (43,44). These tip structures are complex, composed of a network of interactive proteins, designated adhesins, and adherence-accessory proteins (Figure 1, [14,43]).

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

Once they attach to a host cell in the body, their unique plasma and protein coating can then mimic the cell wall of the host cell and the immune system can not differentiate the mycoplasma from the body’s own host cell (1).

G. vaginalis was isolated from the vaginal sample by streaking the specimen on a selective human blood Tween (HBT) bilayer agar medium (Becton-Dickinson).

Virulence factors in Escherichia coli urinary tract infection.

Enterococcus 2%

Role of Uropathogenic Escherichia coli Virulence Factors in Development of Urinary Tract Infection and Kidney Damage

The most common viruses detected in the MEF in these studies were RSV, influenza viruses, adenovirus, and parainfluenza viruses, i.e., the same viruses that had been identified in the nasopharyngeal specimens from children with AOM.

Pneumatic otoscopy is the standard of care in the diagnosis of acute and chronic otitis media. In AOM, the tympanic membrane normally demonstrates signs of inflammation, beginning with reddening of the mucosa and progressing to the formation of purulent middle ear effusion and poor tympanic mobility. The tympanic membrane may bulge in the posterior quadrants, and the superficial epithelial layer may exhibit a scalded appearance (see the image below).

Virulence

Trich can cause genital inflammation that makes it easier to become infected with the HIV virus or to pass the HIV virus on to a sex partner.

Recovery of Mycoplasma hominis from blood culture media.

epithelial cells, biofilm production, surface hydrophobicity, phospholipase C and protease activity

Candida albicans

Serratia spp. (4.2%), and Enterobacter spp. (4.2%)

The single most important lab test is urinalysis.

Deaths have occurred in neonates with bloodstream invasion by Ureaplasma species and meningitis caused by M hominis;

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.

Symptoms of lower urinary tract infections usually begin suddenly and may include one or more of the following signs:

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.

Benign prostatic hyperplasia (BPH), enlargement of the prostate gland, can produce obstruction in the urinary tract and increase the risk for infection.

Specific Risk Factors in Women

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 .

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.

Recurrences occur in up to 50 - 60% of patients with complicated UTI if the underlying structural or anatomical abnormalities are not corrected.

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

UTIs are the most common of all bacterial infections and can occur at any time in the life of an individual.

Gardnerella vaginalis, Mycoplasma hominis and various anaerobic bacteria including Mobiluncus sp., and Prevotella sp.

These are primarily anaerobic bacteria and an organism called Gardnerella vaginalis,

E. coli are covered with fimbriae, which are tiny, finger-like appendages that slowly climb up the walls of your urinary tract. Fimbriae are made of lectins, proteins that bond perfectly with mannose — cells that line your urinary tract — making bacteria hard to wash out

xam Overview

herpes simplex virus–1 (HSV-1) and HSV-2

A health care provider will examine your vagina for signs of vaginal discharge. Your provider can also perform laboratory tests on a sample of vaginal fluid to determine if BV is present.

S. pneumoniae, H. influenzae, M. catarrhalis, group A beta-hemolytic streptococci and S. aureus (12, 18, 21–24, 63) (Table 1). The introduction of vaccination of children with the 7-valent pneumococcal vaccine in 2000 in the USA brought about a decline in the incidence of S. pneumoniae and an increase in H. influenzae in sinusitis

Bacterial Vaginosis Workup

Clindamyci

Metronidazole is the most common antibiotic for BV.

fishy smell, bacterial vaginosis is a better guess

The most common types of vaginitis are:

Drug Resistant TB Is Predicted To Steadily Spread In 4 Countries

When 10% ferric chloride is added to phenylalanine deaminase medium inoculated with Proteus mirabilis, the presence of phenylpyruvic acid causes the media to turn dark green.  This is a positive result.

Proteus mirabilisATCC 14153 Growth good to excellent; colonies medium-sized, pale to beige, surrounded by an amber to brown halo; in areas of dense growth, the medium may be completely amber to brown. Swarming is partially to completely inhibited.

Proteus spp. can be naturally resistant to antibiotics, such as benzylepenicillin, oxacillin, tetracycline, and macrolides (137). Proteus spp. can acquire resistance to ampicillin through plasmid mediated beta-lactamases, and chromosomal beta-lactamase expression has now been reported (136).

Deposited Name:Proteus vulgaris Hauser emend. Judicial CommissionProduct Description: Quality control strainMediumATCC® Medium 3: Nutrient agar or nutrient brothGrowth ConditionsTemperature: 37°CAtmosphere: AerobicPropagation Procedure1. Open vial according to enclosed instructions.2. Using a single tube of #3 broth (5 to 6 mL), withdraw approximately 0.5 to 1.0 mL with a Pasteur or1.0 mL pipette. Rehydrate the entire pellet.3. Aseptically transfer this aliquot back into the broth tube. Mix well.4. Use several drops of the suspension to inoculate a #3 agar slant and/or plate.5. Incubate the tubes and plate at 37°C for 24 hours.Colonies on #3 agar are cream, translucent, circular, low convex, entire, and smooth. Swarming occurs withextended incubation. Cells are motile rods in singles and pairs that vary in size

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.

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 ConditionsTemperature: 30.0°CAtmosphere: Aerobic

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.

β-lactam antibiotic

Virulence Factors Of Uropathogenic Proteus

Potential virulence factors of Proteus bacilli.

most Shewanella infections are treated easily by a combination of surgical therapy/drainage and antibiotics

S. putrefaciensT (ATCC 8071)

all S. alga strains produced a hemolytic reaction on sheep blood agar while S. putrefaciens isolates lacked this activity.

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

Isolates that were motile, had oxidative metabolisms, were oxidase and catalase positive, ornithine decarboxylase positive, and DNase positive, and produced H2S on triple sugar iron slants within 72 h of incubation were identified as belonging to the phenospecies S. putrefaciens.

production of hydrogen sulfide gas (H2S) on TSI slants

S. alga causes the most human illnesses and that significant differences exist between these two species regarding resistance to antimicrobial agents, mouse pathogenicity, and certain virulence factors (hemolysis and adhesion).

Contact lens wearers are more prone to bacterial infection, especially with Gram-negative organisms. The contact lens induces hypoxia, increases corneal temperature and decreases tear flow over the corneal surface. The adhering 21 of microorganisms (Staphylococci, Moraxella, Candida) to the contact lens and epithelium 22–24 is aided by mucus and proteins. The risk of developing corneal infections is 9–15 times greater with overnight use of contact lenses compared to daytime use. Aphakic eyes are more prone to microbial keratitis with extended wear soft contact lenses. There is a higher risk of bacterial keratitis with disposable contact lenses used overnight.24 The most common organisms associated with contact lens related bacterial keratitis are Pseudomonas aeruginosa and Staphylococci. Bandage soft contact lenses are more often associated with polymicrobial infections (Staphylococci, Streptococci, Serratia). Extended wear soft cosmetic lenses are more prone to Pseudomonas infections.25While Gram-negative organisms like Pseudomonas, Haemophilus and Moraxella cause infectious keratitis in extended wear cosmetic contact lens users, therapeutic soft contact lens wearers on the other hand are prone to corneal ulcers caused by Gram-positive bacteria especially Streptococci.

marcescensS flexneri