32 Matching Annotations
  1. Jun 2017
    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. phagocytosis and complement-mediated lysis in the nonimmune host. The unencapsulated strains are almost always less invasive; they can, however, produce an inflammatory response in humans, which can lead to many symptoms. Vaccination with Hib conjugate vaccine is effective in preventing Hib infection, but does not prevent infection with NTHi strains.[4]

      Haemophilus virulence factors

    1. Sinusitis This is infection of the sinuses. Symptoms in younger children may include: Runny nose that lasts longer than 10 to 14 days. Nasal fluid may become thick green, yellow, or blood-tinged. Nighttime cough Occasional daytime cough Swelling around the eyes Symptoms of sinusitis in older children may include: Runny nose or cold symptoms that last longer than 10 to 14 days Nasal fluid that drains down the back of the throat (postnasal drip) Headache Pain over the cheek bones or over the eyes that’s worse when leaning over (sinus pain) Bad breath Cough Fever Sore throat Swelling around the eye that’s worse in the morning

      Sinusitis symptoms Haemophilus

    1. Fluoroquinolones, and a newer macrolide antibiotic such as clarithromycin or a tetracycline like doxycycline, are used in those who have severe allergies to penicillins.[49] Because of increasing resistance to amoxicillin the 2012 guideline of the Infectious Diseases Society of America recommends amoxicillin-clavulanate as the initial treatment of choice for bacterial sinusitis.[50] The guidelines also recommend against other commonly used antibiotics, including azithromycin, clarithromycin and trimethoprim/sulfamethoxazole, because of growing drug resistance. The FDA recommends against the use of fluoroquinolones when other options are available due to higher risks of serious side effects.[51]

      Talks about additional antibiotic treatment, also possible resistances

    2. if symptoms do not resolve within 10 days, amoxicillin is a reasonable antibiotic to use first for treatment

      Antibiotics used only for cases of bacterial sinusitis, also antibtiocis aren't needed for mild cases

    3. Recommended treatments for most cases of sinusitis include rest and drinking enough water to thin the mucus.[44] Antibiotics are not recommended for most cases.[44] Breathing low-temperature steam such as from a hot shower or gargling can relieve symptoms.[44][45] There is tentative evidence for nasal irrigation.[4] Decongestant nasal sprays containing oxymetazoline may provide relief, but these medications should not be used for more than the recommended period. Longer use may cause rebound sinusitis.[46] It is unclear if nasal irrigation, antihistamines, or decongestants work in children with acute sinusitis.[

      This is more for treating symptoms of sinusitis, but I thought this may be relevant

    4. Recommended treatments for most cases of sinusitis include rest and drinking enough water to thin the mucus.[44] Antibiotics are not recommended for most cases

      Treagment for sinusitis

    5. the most common three causative agents are Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis.[27] Until recently, Haemophilus influenzae was the most common bacterial agent to cause sinus infections. However, introduction of the H. influenza type B (Hib) vaccine has dramatically decreased H. influenza type B infections and now non-typable H. influenza (NTHI) are predominantly seen in clinics. Other sinusitis-causing bacterial pathogens include Staphylococcus aureus and other streptococci species, anaerobic bacteria and, less commonly, gram negative bacteria.

      list of possible organisms that cause disease

  2. May 2017
    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. The most common symptoms of Salmonella Enteritidis include fever, diarrhea, vomiting, abdominal cramps, muscle aches, and headache. These symptoms generally occur between 12-72 hours after the bacteria has been ingested and last anywhere from 4-7 days. Healthy individuals can usually rid themselves of the bacteria on their own; however, children, elderly people, and those with compromised immune systems may require additional treatment [18].

      Clinical manifestations of Salmonella enterica along with who are going to be most susceptible

    2. Once established in the intestine, the bacteria's virulence factors go to work. An enterotoxin results in the release of fluids from the cell into the lumen. This factor is responsible for the diarrhea and vomiting symptoms. Next, the endotoxin results in the release of endogenous pyrogens from the host cell, causing a fever in the victim. Lastly, the cytotoxin is responsible for the disintegration of the cytoplasm.

      virulence factors on how Salmonella enterica causes diarreah

    1. Salmonella can also actively invade both phagocytic and non-phagocytic cells using a type III secretion system (T3SS), T3SS1.

      how it gets into cell

    1. The main habitat where Salmonella is found is in the intestines of animals and humans (figure 4). Typical vectors of Salmonella enterica include chicken including their eggs, swine, dairy and beef cattle, and sometimes even insects, rodents, and other farm animals.

      where they are found

    1. There were 216 gastroenteritis cases reported from 20 November to 4 December 2007. The causative agent was identified as Salmonella enterica subspecies enterica serotype Enteritidis for 14 out of 20 cases tested. The vehicle of transmission was traced to cream cakes produced by a bakery and sold at its retail outlets (P < 0.001, OR = 143.00, 95% Cl = 27.23–759.10). More than two-thirds of the 40 Salmonella strains isolated from hospitalized cases, food samples and asymptomatic food handlers were of phage type 1; the others reacted but did not conform to any phage type. The phage types correlated well with their unique antibiograms. The ribotype patterns of 22 selected isolates tested were highly similar, indicating genetic relatedness. The dendrogram of the strains from the outbreak showed distinct clustering and correlation compared to the non-outbreak strains, confirming a common source of infection.

      some outbreak statistics

    1. Local Cases/Outbreaks:             In 2006, University Hospital located in San Antonio, Texas saw an increase in P. aeruginosa infections in its neonatal intensive care unit, leading for a study to be conducted with data ranging from 2005 to 2007. [11] This unit generally has a low incidence of this pathogen and has seen fewer cases since revision of control measures. [11] The patients with this infection tended to be male and had received mechanical ventilation at one point. [11] During the study, 23 patients were confirmed with P. aeruginosa. Only 13% of patients were antibiotic resistance and 30% of the patients died. [11] In US hospitals, there are about 4 per 1000 discharges (0.4%) of P. aeruginosa infections. [3] Approximately 10.1% of nosocomial infections result due to this bacterium. [3] Also, this pathogen is responsible for about 16% of hospital acquired pneumonia, 12% of urinary tract nosocomial infections, 8% of surgical wound infections, and 10% of bacteremia infections. [2]   Global Cases/Outbreaks:             An outbreak in a Warsaw, Poland hospital saw 41 P. aeruginosa cases with PER-1 extended spectrum beta-lastamase. This clonal complex is normally seen in Turkey but has now been identified in the far eastern countries and Europe. In Greece, there was a hospital outbreak of multiple strains of this pathogen, which carried two metallo beta-lactamase gene variants. [13] Pseudomonas pneumonia is a common infection found in most hospitals throughout the world.

      Outbreak stats

    2. Tissue damage caused by proteases and toxins invade blood vessels causing a systemic inflammatory response, dissemination to other organs that may lead to multiple organ failure and possibly death. [2] The two hemolysins produced by this bacterium may act together in breaking down lipids and lecins along with tissue damage caused by the cytotoxins. The next stage after the acute infection is the chronic phase but  this stage can also happen directly after colonization. The chronic infection has selected alginate yielding mutants, protects from host immunity, has a low production of extracellular virulence factors, and the tissue damage is chiefly caused by the chronic inflammation process.  

      Virulence Factors

    1. RESULTS: Twelve patients with a culture positive for P. aeruginosa with the unique susceptibility pattern were identified in June-July 2007. No cases were documented from March 1 through May 31, 2007. Culture specimens obtained from B1 after high-level disinfection revealed P. aeruginosa, prompting removal of B1 from service on July 23, 2007. No cases occurred after that date. Eleven (55%) of 20 patients who were exposed to B1 during the cluster period had a culture positive for P. aeruginosa, compared with 1 (2%) of 53 patients who were exposed to other bronchoscopes (P < .001). PFGE patterns for P. aeruginosa isolates obtained from case patients and from B1 were identical. An engineering evaluation of B1 documented several internal damages. Two (10.5%) of 19 patients exposed to B1 during the cluster period may have developed P. aeruginosa infection following exposure to B1.

      Possible outbreak stuff

    1. Antibiotic susceptibility patterns of thirty-seven isolates of Fusobacterium necrophorum (21 biotype A and 16 biotype B) from liver abscesses of feedlot cattle were determined. These isolates were generally susceptible to penicillins, tetracyclines (chlortetracycline and oxytetracycline), lincosamides (clindamycin and lincomycin), and macrolides (tylosin and erythromycin) but resistant to aminoglycosides (kanamycin, neomycin, gentamycin and streptomycin), ionophores(except narasin), and peptides (avoparcin, polymixin, and thiopeptin). Differences in antibiotic sensitivity patterns were observed between the two biotypes

      For q4 on case 2 assessment

    1. group B streptococci to be sensitive to ceftriazone in vitro and that, in the low dosage used, ceftriaxone effectively eradicates group B streptococcal bacteraemia and meningitis in infant rats.

      Ceftriaxone can be used to treat the patient

    1. Pharyngitis — Gonococcal infection of the pharynx is usually acquired by oral sexual exposure [42]; it is acquired more efficiently by fellatio than by cunnilingus [27,42]. Based on studies of women presenting to sexually transmitted infection (STI) clinics, the prevalence of pharyngeal gonorrhea has been estimated at two to six percent [43,44]. In a study of over 14,000 men who have sex with men (MSM) presenting to STI clinics in the United States, eight percent tested positive for pharyngeal gonococcal infection [34].The majority of oropharyngeal infections with N. gonorrhoeae are asymptomatic, although sore throat, pharyngeal exudates, and/or cervical lymphadenitis are present in some cases. In a study of 192 men and women seeking care for sore throat in a general medicine setting, one percent overall had a positive throat culture for N. gonorrhoeae [45]. Although bacterial concentrations in the pharynx are generally lower than in the rectum and genitals, the pharynx is thought to be the site where horizontal transfer of gonococcal antimicrobial resistance genes commonly occurs [46].

      could be useful during the case assessment

    1. Because the gastrointestinal tract is a primary source of this organism, the appropriate specimens for culture are a vaginal swab and a rectal swab. The specimens should be cultured using a selective enrichment broth.

      how to culture GBS

    2. Streak for isolation and incubate at 35-37o C in ambient air or CO2 for 18-24 hours.

      Culture instructions

  3. Apr 2017
    1. major use of vancomycin today is for infections caused by methicillin-resistant Staphylococcus aureus (MRSA), methicillin-resistant Staphylococcus epidermidis (MRSE) and amoxicillin-resistant enterococci. In its oral form, vancomycin is used to treat diarrhea caused by Clsotridium difficile.

      Vancomycin can be used to tackle MRSA (Methicillin Resistant Staph Aureus) and MRSE (Methicillin Resistant Staph Epidermidis)

    1. This type of medium is both selective and differential. The MSA will select for organisms such as Staphylococcus species which can live in areas of high salt concentration (plate on the left in the picture below). This is in contrast to Streptococcus species, whose growth is selected against by this high salt agar (plate on the right in the picture below).
    1. The bile-esculin test is used to differentiate enterococci and group D streptococci from non-group D viridans group streptococci. The effects on test performance of the concentration of bile salts, inoculum, and duration of incubation were examined with 110 strains of enterococci, 30 strains of Streptococcus bovis, and 110 strains of non-group D viridans group streptococci. Optimal sensitivity (>99%) and specificity (97%) of the bile-esculin test can be obtained with a bile concentration of 40%, a standardized inoculum of 106 CFU, and incubation for 24 h.

      This is what I found on Bile Esculin Test

    1. The first sign of this infection is a blister or a small bump that develops several days after the scratch or bite and may resemble a bug bite. This blister or bump is called an inoculation lesion (a wound at the site where the bacteria enter the body). Lesions are most commonly found on the arms and hands, head, or scalp and usually are not painful.

      Has the friend noticed any unusual lumps or blisters on their body, specifically the armpit region?

    2. n the United States, most cases happen in the fall and winter and usually affect kids, probably because they're more likely to play with cats and be bitten or scratched

      Is the friend our age? Also have they been exposed to a cat recently and have they come into physical contact with said cat?

    1. There are a number of possible complications from cat scratch fever.

      Could be possible examples of Sequelae for Cat Scratch Disease