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

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.

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The six cases involving S. putrefaciens were regarded as colonisations and were consequently not treated with specific antibiotics

eye infections [1,16].

S. algae and S. putrefaciens are non-fermentative bacilli with a single polar flagellum. They grow well on conventional solid media, including MacConkey agar, with 1–2-mm yellowish-brown colonies after incubation for 18–24 h.

An ability to form biofilms has been described in detail for Shewanella oneidensis and S. putrefaciens

en TSTs wer

Gastroenteritis: Gastroenteritis or “food poisoning” is usually characterized by sudden nausea, vomiting, abdominal cramps, diarrhea, headache chills and fever up to 39 ºC (6-9). The symptoms can be mild to severe and may last between 5-7 days (7, 8). The Typhimurium serotype is the most common cause of gastroenteritis and there are an estimated 1.3 billion cases and 3 million deaths annually (1.4 million cases and 600 deaths in the US alone) due to non-typhoidal Salmonella (2, 9, 10). In well resourced countries with low levels of invasive complications, the mortality rate due to non-typhoidal Salmonella is lower then 1% (10); however, in developing countries, the mortality rate can be as high as 24%

The usual habitat for subspecies II, IIIa, IIIb, IV and VI is cold-blooded animals and the environment (2). All species of Salmonella can infect humans.

Amoxicillin/clavulanate

Evasion of mucosal immunity

Hib pneumonia: Clinically indistinguishable from other bacterial pneumonias—except for its insidious onset and a history of fever, cough, and purulent sputum production

isolation from clinical specimens on solid medium requires the use of chocolate agar or other X and V factor supplemented media.

The most common types of disease caused by H. influenzae type b (Hib) include pneumonia, bacteremia, meningitis, epiglottitis, septic arthritis, cellulitis, otitis media, purulent pericarditis, and other less common infections such as endocarditis and osteomyelitis. Non-b H. influenzae can cause disease similar to Hib infections. Nontypeable H. influenzae commonly causes ear infections in children and bronchitis in adults, but also causes invasive disease, such as bacteremia and bacteremic pneumonia.

H. influenzae, including Hib, are spread person-to-person through respiratory droplets that occur when someone who has the bacteria in their nose or throat coughs or sneezes.

H. influenzae, including Hib, disease occurs mostly in babies and children younger than five years old. Adults 65 years or older, American Indians, and Alaska Natives are also at increased risk for getting sick with invasive H. influenzae disease.

Disseminated gonococcal infection

Role of Pili in the Virulence of Neisseria gonorrhoeae

Mechanisms of Resistance to Fluoroquinolones Fluoroquinolones inhibit the replication of DNA; they are believed to bind to the GyrA region of DNA gyrase, which is attached to DNA, and inhibit the enzyme from supercoiling the DNA (37). Resistance to fluoroquinolones in N. gonorrhoeae is associated with mutations that result in amino acid changes in the A subunit (GyrA) and the B subunit (GyrB) of the DNA gyrase, and in the parC-encoded subunit of topoisomerase IV (37-40). Although mutations in gyrB confer low-level resistance to naladixic acid, high-level quinolone resistance is associated with mutations in the quinolone resistance-determining region of gyrA (41). Topoisomerase IV, encoded by parC and parE in Escherichia coli and believed to be located in the cytoplasmic membrane, is involved in DNA replication but is not as sensitive to fluoroquinolone inhibition as is DNA gyrase (37). No parE analog has been detected in N. gonorrhoeae (37). Mutations in gyrA and parC are most relevant when considering clinically significant levels of fluoroquinolone resistance in N. gonorrhoeae (37,39,40). Similar results have been obtained in studies of gyrA mutations in both laboratory-adapted strains and clinical isolates (37,39,40): ciprofloxacin-susceptible strains (MICs, <0.03 µg/ml) had no mutations in gyrA and strains with MICs, ≥0.5 µg/ml of ciprofloxacin may have changes in nucleotides 272 and 283 of gyrA. In addition, strains with MICs ≥2.0 had mutations in parC. Mutations in parC were observed only in strains with at least one mutation in gyrA (37,39) and appeared to be associated with an MIC higher than would be expected with the gyrA mutation alone (39). Mutations in gyrA and parC may be characterized by polymerase chain reaction and DNA sequencing (37,39). The transfer of gyrA and parC mutations between gonococcal strains has been demonstrated in vitro (37). The presence of transformation sequences just downstream from the gyrA sequences suggests that transformation may play a role in the spread of gyrA mutations between gonococcal strains in vivo (37). The opportunity for transformation of genes between gonococcal strains, which depends on concurrent infections with multiple strains, has been documented for women and homosexual men (42,43).

Neisseria models of infection and persistence in the upper respiratory tract

This is another picture of a blood agar plate with growth and hemolytic activity of group B streptococci (GBS) (on the left) and group A streptococci (GAS) (on the right). Note that the colonies of both bacteria appear about the same color and size, but the degree of hemolytic activity is very different. The group A Streptococcus has more hemolytic activity than the group B Streptococcus. Experienced microbiologist use these traits to identify the two types of bacteria.

APACHE scores

osteomyelitis

Earlier on, vancomycin was associated with many side effects including vestibular and renal,

ests for clumping factor, coagulase, hemolysins and thermostable deoxyribonuclease are routinely used to identify S aureus. Commercial latex agglutination tests are available. Identification of S epidermidis is confirmed by commercial biotyping kits.

Streptomycin

Typhoidal

Pneumonic

Oropharyngeal

Oculoglandular

Glandular

Ulceroglandular

Tick and deer fly bites Skin contact with infected animals Ingestion of contaminated water Inhalation of contaminated aerosols or agricultural dusts Laboratory exposure

Francisella tularensis

bat species

super-shedders

cleared Dugas' name and provided strong evidence that the virus emerged in the United States from a pre-existing Caribbean epidemic in or around 1970.

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