1,440 Matching Annotations
  1. Jun 2017
    1. Epidemiology

      this is global

    2. Disease: Signs and Symptoms

      not really global...more infection/organismal.

    3. Southeast Asia

      Both NiV and Rubeola have a high prevalence in South East Asia. For NiV, the outbreak is contained to Malaysia (for now), whereas Rubeola has been eliminated from the US and other developed nations thanks to vaccination, leaving SEA as the area with the highest prevalence.

    4. encephalitis

      Both Rubeola and NiV can cause encephalitis. Every documented case of NiV has reported some form of encephalitis while 1/1000 cases of Rubeola cause encephalitis.

    1. Humans are the primary reservoir for the HSV-1 virus

      CCHFV reservoir is ticks, while the HSV1 reservoir is humans.

    2. The prevalence is highest in Africa (87%)

      Both CCHFV and HSV1 have the highest prevalence in Africa.

    3. Introduction

      Both Herpes Simplex Virus 1 and Mumps show symptoms including stomatitis (inflammation of the mucosal surfaces in the mouth and on the tongue). https://www.atsu.edu/faculty/chamberlain/website/lectures/lecture/mumps.htm

    4. Immunocompromised people are at risk of getting keratitis or encephalitis

      Both Mumps Virus and Herpes Simplex Virus 1 can infect the cerebrospinal fluid, penetrating the brain and causing encephalitis.

    1. 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.

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

      Both CCHFV and HSV1 have the highest prevalence in Africa.

    3. Mechanism of Viral Protein Synthesis and Replication

      Both CCHF and Norovirus utilize host machinery to undergo translation and they both have negative-sense, single stranded RNA while replicating their genome. Norovirus has positive sense single stranded RNA, but during replication converts it into negative sense ssRNA.

    4. Vaccination, Treatment & Public Health Concerns

      Treatment for both CCHF and Norovirus are symptomatic. Both are treated with fluid replenishing given through an IV.

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

      Rate of organism causing sepsis

    1. parotid glands

      Both Herpes Simplex Virus 1 and Mumps show symptoms including stomatitis (inflammation of the mucosal surfaces in the mouth and on the tongue). https://www.atsu.edu/faculty/chamberlain/website/lectures/lecture/mumps.htm

    2. 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).

      Both Mumps Virus and Herpes Simplex Virus 1 can infect the cerebrospinal fluid, penetrating the brain and causing encephalitis.

    1. HPV infection has been known to progress to cancer

      Both HPV and Hepatitis C virus can cause different types of cancer.

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

      Both HPV and Hepatitis C virus can enter the host through broken skin.

    3. 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 primarily targets the basal cells of the epithelium, while rotatvirus targets the apical epithelial cells at the tips of villi.

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

      Both HPV and rotavirus enter the cell through endocytic pathways.

    1. HCV causes mortality in the form of hepatitis and liver cancer

      HPV and Hepatitis C virus can cause different forms of cancer.

    2. 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

      Both HPV and Hepatitis C virus can cause infection through a broken skin

    1. 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.

      could happen not likely though

    1. South East Asia

      Both NiV and Rubeola have a high prevalence in South East Asia. For NiV, the outbreak is contained to Malaysia (for now), whereas Rubeola has been eliminated from the US and other developed nations thanks to vaccination, leaving SEA as the area with the highest prevalence.

    2. encephalitis

      Both Rubeola and NiV can cause encephalitis. Every documented case of NiV has reported some form of encephalitis while 1/1000 cases of Rubeola cause encephalitis.

    3. spreads through the air

      MMR can spread indirectly by air, but Ebola does not.

    4. synthesize a positive-strand antigenome,

      Both MMR and Ebola synthesize a positive-strand antigenome.

    5. 97% effective vaccine MMR

      MMR has a vaccine available, but not Ebola.

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

      Both HPIV and EBV have no known vaccinations and both can be found the respiratory tracts of humans.

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

      Both HPIV and Epstein-Barr Virus (EBV) have no known vaccinations and can both be found in the respiratory tract of humans.

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

      Mosquitos are the main mode of transmission in both Yellow fever Virus and Zika Virus.

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

      Both Yellow Fever Virus and Zika Virus lack a 3' poly(A) tail in their genomic mRNA.

    1. Spread by mosquitoes

      Mosquitos are the main mode of transmission in both Yellow fever Virus and Zika Virus.

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

      Both Yellow Fever Virus and Zika Virus lack a 3' poly(A) tail in their genomic RNA structure.

    1. Global Public

      The Ebola virus and the influenza virus can both be spread through contact with bodily fluids. Both viruses also encode their genomes on negative single-stranded RNA.

    2. receptor-mediated endocytosis

      entry

    3. 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,

      reservoir - animals

    1. Ebola

      The Ebola virus and the influenza virus can both be spread through contact with bodily fluids. Both viruses also encode their genomes on negative single-stranded RNA.

    1. fever,

      Both the Lassa Virus and the Respiratory Syncytial Virus cause fevers.

    2. 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.

      Both the Lassa virus and the Respiratory syncytial virus contain a negative sense genome. However, the Lassa virus genome has two RNA strands, while the RSV genome has only one.

    1. fever

      Both the Lassa Virus and the Respiratory Syncytial Virus cause fevers.

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

      Both the Lassa virus and the Respiratory syncytial virus contain a negative sense genome. However, the Lassa virus genome has two RNA strands, while the RSV genome has only one.

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

      RSV REPLICATION MECHANISM

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

      RSV Portal of Entry

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

      RSV NOSOCOMIAL SPREAD

    6. human contact from the spread of infected respiratory secretions like mucous

      RSV Mode of Transmission

    1. human-human contact

      Ebola is transmitted by direct contact, but MMR includes indirect contact by air.

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

      EBOLA REPLICATION MECHANISM

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

      EBOLA Portal of Entry

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

      EBOLA Resevoir

    5. 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

      Ebola - NOSOCOMIAL SPREAD

    6. 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

      Ebola Mode of Transmission

    1. Genomic Replication Cycle

      Both the zika virus and the yellow fever virus are positive sense RNA viruses that use host cell machinery to replicate its own genomic material. Both of these viruses are also transmittd through Aedes aegypti mosquitos (vector).

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

      These are coded in the polyprotein, a hallmark of flaviviruses, but also seen in Human Rhinovirus, as the polyprotein codes similrly for 11 proteins, some functioning as replication complex.

    3. single stranded RNA that is positively charged

      This extend beyond the flaviviruses and is also seen in Human Rhinovirus.

    1. Part 3: Zika Replication

      Both the zika virus and the yellow fever virus are positive sense RNA viruses that use host cell machinery to replicate its own genomic material. Both of these viruses are also transmittd through Aedes aegypti mosquitos (vector).

    1. receptor-mediated endocytosis begins

      Both West Nile Virus and Norovirus enter the cell through receptor-mediated endocytosis

    2. positive-sense single stranded RNA

      Both West Nile Virus and Norovirus have a genome structured as positive-sense single-stranded RNA

    1. Internalized

      Both West Nile Virus and Norovirus enter the cell through receptor-mediated endocytosis

    2. Positive-sense RNA strand ((+)RNA)

      Both West Nile Virus and Norovirus have a genome structured as positive-sense single-stranded RNA

    1. translated protein gets cleaved by virally encoded proteases and then yields

      Coding for a single polyprotein is also common for flaviviruses like Human Rhinovirus, and then getting cleaved into proteins that assist in replication process.

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

      This is also shared with the flaviviruses, which includes Human Rhinovirus.

    1. joint pain,

      Both Dengue Virus and Chikungunya can cause Joint Pain, but Chikungunya virus can cause joint pain that can lasts months to years mimicking cases of rheumatoid arthritis

    2. 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)

      Both Dengue Virus and Chikungunya are spread via the Aedes aegypti mosquito, but the Chikungunya virus can also be spread by Aedes albopticus mosquito.

    1. joint pain

      Both Dengue Virus and Chikungunya can cause Joint Pain, but Chikungunya virus can cause joint pain that can lasts months to years mimicking cases of rheumatoid arthritis

    2. mosquito vector bites an infected viral reservoir

      Both Dengue Virus and Chikungunya are spread via the Aedes aegypti mosquito, but the Chikungunya virus can also be spread by Aedes albopticus mosquito

    1. initiate entry into the host cell via receptor mediated endocytosis

      Both HPV and rotavirus enter the cell through endocytic pathways.

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

      HPV primarily targets the basal cells of the epithelium, while rotatvirus targets the apical epithelial cells at the tips of villi.

    1. human monoclonal antibodies that target Nipah G glycoprotein

      Just like Marburg virus can cause fever and headaches

    2. To date, there are no known vaccines.

      Just like Marburg virus there are no vaccines for Nipah virus.

    3. typically fever and  a headache

      Both Nipah and Marbug viruses cause fever and headache.

    1. Currently, there is no vaccine for the Marburg viru

      Just like the Nipah Virus there is no vaccine but there are steps being taken to stop the sympotomology such as the use of small interfering RNA (Marburg) and human monoclonal antibodies that target G glycoprotein

    2. tissue, body fluids, and secretions

      The marburg and Nipah viruses exit adn enter the host through mucus membranes and eating foods which have eaten which was in contact with the animal.

    3. The Marburg virus is zoonotic,

      Both this virus and Nipah virus are zoonotic both found in fruit bats. Nipah can only be spread from animals which are alive while Marburg can spread even if the animal is dead.

    1. 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

      cytoplasmic inclusion body in replication

    2. 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).

      glycoproteins and receptor mediated endocytosis

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

      reservoir - animals

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

      Both LCMV (RNA) and Smallpox Virus (DNA) replicate their genome in the cytoplasm.

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

      LCMV is transmitted from mouse to human and Smallpox Virus is transmitted from human-human.

    1. Treatment

      Treatment for both CCHF and Norovirus are symptomatic. Both are treated with fluid replenishing given through an IV.

    2. Mechanism of Viral Replication

      Both CCHF and Norovirus utilize host machinery to undergo translation and they both have negative-sense, single stranded RNA while replicating their genome. Norovirus has positive sense single stranded RNA, but during replication converts it into negative sense ssRNA.

    1. genome

      Crimean-Congo Hemorrhagic Fever Virus is a negative-sense, single strand RNA virus, but HIV is a positive-sense single strand RNA virus.

    2. zoonotic transmission

      Both Crimean-Congo Hemorrhagic Fever Virus and HIV have non-human reservoirs.

    1. including the common cold, bronchitis, pneumonia,

      Adenovirus and Sin Nombre Virus can both cause respiratory disease

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

      Adenovirus and Sin Nombre Virus both use integrin proteins to complete receptor-mediated endocytosis

    1. negative-sense, single-stranded RNA genome

      Crimean-Congo Hemorrhagic Fever Virus is a negative-sense, single strand RNA virus, but HIV is a positive-sense single strand RNA virus.

    2. ticks infected with CCHFV

      Both Crimean-Congo Hemorrhagic Fever Virus and HIV have non-human reservoirs.

    1. which progresses to a severe respiratory disease

      Adenovirus and Sin Nombre Virus can both cause respiratory disease

    2. 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).

      Adenovirus and Sin Nombre virus both use integrin proteins to complete receptor-mediated endocytosis

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

      The transmission of varicella zoster virus is unlike the transmission of West Nile virus, which primarily occurs through mosquito bites and does not spread from casual contact from person-to-person (West Nile virus can be spread from contact with infected blood and from mother to child during birth or through breastmilk).

    2. probably involves either endocytosis

      West Nile virus is taken up into human cells via receptor-mediated endocytosis, similar to the proposed entry method of endocytosis for varicella zoster virus.

    3. being neurotropic

      Varicella zoster virus and West Nile virus are both neurotropic pathogens.

    1. cell surface

      maybe start with which cells before you talk about molecules.

    2. symptomatically

      I don't think you mean to say it like this

    3. luctuating climates

      what does this mean? be specific

    4. recently

      give a date or change this to say "recent outbreak"

    5. transmission

      I don't think you mean "transmission" here

    6. The initial symptoms o

      rather than start with symptoms (organismal), talk about distribution prevalence, etc first.

    7. Enterovirus genus

      put references at the end of your sentences

    8. categorized alongside poliovirus

      say "is similar to"

    1. ers into the cell's cytosol.

      please refer to the figures so your reader knows when to look

    2. RME

      since you never use this again, there is no reason to make an acronym

    1. Caroline Beuligmann

      lovely!

    2. 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).

      put the image reference here or better yet...stick the image here.

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

      start with this statement since you really want to emphasize that anyone can get it.

    4. a (See Figure 1 and Table 2)

      I suggest you set this up better so that the TWO images you insert to talk about outbreaks is given more weight in your text.

    1. released via budding.

      maybe bring back to the virus is now ready to infect a new cell

    2. hree proteins—P, V, and C.

      refer to figure here...makes your life so much easier

    3. Life cycle of the measles virus

      maybe put this as the first image since it is an overview.

    1. lipid rafts

      I don't think many people know what these are. you may want to include this concept in the figure 2

    2. peplomers

      I have never heard this before...how different from proteins?

    3. see figure 1

      This figure is at the molecular level...can you get a picture of the virus?

    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

      acquired resistance

    1. 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.

      HIB in otitis media

    1. 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).

      virulence - biofilm production by Gardnerella vaginalis & Mobiluncus mulieris

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

      adherence, biofilm, cytotoxicity

      virulence factors for G. vaginalis

    1. 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]).

      Mycoplasma virulence - specialized polar tip organelles

    1. 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

    1. 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).

      virulence, Mycoplasma

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

      Virulence factors UTI, E coli

    1. 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.

      Viral antigens in AOM

    1. 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).

      AOM clinical presentation and material for diagnosis

  2. May 2017
    1. 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.

      complications of parasitic vaginitis (trichomoniasis)

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

      mortality information

    1. 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

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

      symptoms

    3. 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

    4. 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

    5. Specific Risk Factors in Women

      risk factors

    6. 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

    7. 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

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

      recurrence

    9. 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

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

      prevalence

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

      Other probabe causative organism

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

      A possible caustative organism. No one really knows for sure.

    1. 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

      viruelence factor e. coli

    1. 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.

      test vaginal fluid to determine for presence of bacterial vaginosis

  3. onlinelibrary.wiley.com onlinelibrary.wiley.com
    1. 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

      Common bacterial causes

    1. Clindamyci

      Alternative treatments if metronidazole does not work. If it comes back despite using clindamycin, use tinidazole.

    2. Metronidazole is the most common antibiotic for BV.

      Most common form of treatment for bacterial vaginitis.

    1. 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.

      phenylalanine deaminase test for Proteus mirabilis - dark green color change (positive)

    1. 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 mirabilis growth on CHROMagar (Orientation)

    1. 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).

      More info on resistances

    1. 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

      Proteus vulgaris growth conditions + colony morphology on nutrient agar (type of non-selective growth media)

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    1. 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

    1. 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

    1. Growth ConditionsTemperature: 30.0°CAtmosphere: Aerobic

      growth conditions

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    1. 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

    2. β-lactam antibiotic

      mechanism of action

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

      no hemolysis for S. putrefaciens

    2. 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

    3. 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.
    4. production of hydrogen sulfide gas (H2S) on TSI slants

      Main identifyer

    5. 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).

      S. alga is usually the disease culprit