HPV infection has been known to progress to cancer

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

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

Marburg haemorrhagic fever

Risk factors

Marburg virus disease

Marburg virus

Host Cell Factors in Filovirus Entry: Novel Players, New Insights

Ebola virus entry requires the cholesterol transporter Niemann-Pick C1

Cellular Entry of Ebola Virus Involves Uptake by a Macropinocytosis-Like Mechanism and Subsequent Trafficking through Early and Late Endosomes

Tissue and cellular tropism, pathology and pathogenesis of Ebola and Marburg viruses

Ebola and Marburg haemorrhagic fever

Outbreaks Chronology: Marburg Hemorrhagic Fever

Filovirus Tropism: Cellular Molecules for Viral Entry

Characterization of nalidixic acid and ciprofloxacin resistance mechanisms in isolates from Bangladesh.The 38 isolates from Bangladesh were categorized into the following 5 ciprofloxacin susceptibility groups: a susceptible group, with MICs of ≤0.03 μg/ml; a group with reduced susceptibility, with MICs of 0.12 to 0.5 μg/ml; and resistant groups, with MICs of 4 μg/ml, 8 μg/ml, and 16 μg/ml (Table 3). The isolates with reduced susceptibility to ciprofloxacin were resistant to nalidixic acid (MICs of 128 to 256 μg/ml), and the trait of resistance was associated with a mutation in gyrase subunit A (S83F, S83Y, or D87N) and enhanced activity of the efflux pump for nalidixic acid. The isolates with a ciprofloxacin MIC of 4 μg/ml were highly resistant to nalidixic acid (MICs of ≥256 μg/ml), and the resistance was associated with a mutation (S83Y) in gyrase A, the presence of qnrS, and enhanced activity of the efflux pumps for ciprofloxacin and nalidixic acid. The isolates with ciprofloxacin MICs of 8 and 16 μg/ml also displayed high nalidixic acid resistance (MICs of >256 μg/ml), carried two mutations (S83F and D87G) in gyrase A and one mutation (E92K) in topoisomerase IV, and showed enhanced efflux pump activity for nalidixic acid. The isolates with a ciprofloxacin MIC of 16 μg/ml also showed enhanced efflux pump activity for ciprofloxacin.

RESISTANCE OF CONCERN

Evaluation of Biofilm Formation Among Klebsiella pneumoniae Isolates and Molecular Characterization by ERIC-PCR

Klebsiella pneumoniae is a Gram-negative, nonmotile, encapsulated, lactose-fermenting, facultative anaerobic, rod-shaped bacterium. It appears as a mucoid lactose fermenter on MacConkey agar.

If the specific Klebsiella in a particular patient does not show antibiotic resistance, then the antibiotics used to treat such susceptible isolates include ampicillin/sulbactam, piperacillin/tazobactam, ticarcillin/clavulanate, ceftazidime, cefepime, levofloxacin, norfloxacin, gatifloxacin, moxifloxacin, meropenem, and ertapenem. Some experts recommend the use of meropenem for patients with ESBL-producing Klebsiella. The claim is that meropenem produces the best bacterial clearing.

A number of mechanisms cause carbapenem resistance in the Enterobacteriaceae. These include hyperproduction of ampC beta-lactamase with an outer membrane porin mutation, CTX-M extended-spectrum beta-lactamase with a porin mutation or drug efflux, and carbapenemase production. The most important mechanism of resistance by CRKP is the production of a carbapenemase enzyme, blakpc. The gene that encodes the blakpc enzyme is carried on a mobile piece of genetic material (a transposon; the specific transposon involved is called Tn4401), which increases the risk for dissemination. CRE can be difficult to detect because some strains that harbor blakpc have minimum inhibitory concentrations that are elevated, but still within the susceptible range for carbapenems. Because these strains are susceptible to carbapenems, they are not identified as potential clinical or infection control risks using standard susceptibility testing guidelines. Patients with unrecognized CRKP colonization have been reservoirs for transmission during nosocomial outbreaks. Depending on the type of infection and the mode of infectivity, cells of Klebsiella spp. may adhere and attack upper respiratory tract epithelial cells, cells in gastrointestinal tract, endothelial cells, or uroepithelial cells, followed by colonization of mucosal membranes (phac-aspc.gc.ca).[15]

Klebsiella organisms are often resistant to multiple antibiotics. Current evidence implicates plasmids as the primary source of the resistance genes.[9] Klebsiella species with the ability to produce extended-spectrum beta-lactamases (ESBL) are resistant to many classes of antibiotics. The most frequent are resistance to aminoglycosides, fluoroquinolones, tetracyclines, chloramphenicol, and trimethoprim/sulfamethoxazole.[10]

alcoholism

As a general rule, Klebsiella infections are seen mostly in people with a weakened immune system. Most often, illness affects middle-aged and older men with debilitating diseases. This patient population is believed to have impaired respiratory host defenses, including persons with diabetes, alcoholism, malignancy, liver disease, chronic obstructive pulmonary diseases, glucocorticoid therapy, renal failure, and certain occupational exposures (such as papermill workers). Many of these infections are obtained when a person is in the hospital for some other reason (a nosocomial infection). Feces are the most significant source of patient infection, followed by contact with contaminated instruments.[citation needed]

Group B streptococcus (strep) is a common bacterium often carried in your intestines or lower genital tract. Group B strep is usually harmless in adults. In newborns, however, it can cause a serious illness known as group B strep disease.

penicillin

Carriage and transmission of group A streptococci

Numerous epidemiological studies have identified high rates of invasive S. pyogenes infection in men rather than women, a pattern that can be observed for many other invasive bacterial infections and one that is not fully understood. Age-specific incidence rates show a typical J-shaped distribution, with highest rates in the elderly, followed by infants. Assessment of rates of disease according to patient ethnicity show generally higher rates of disease in individuals of non-white European descent. These observations have been made in a diverse range of populations, including indigenous populations of Australia, New Zealand, the Pacific Islands, and circumpolar regions of the northern hemisphere. The reasons behind these excesses in risk are poorly understood and could reflect differential access to healthcare or general living conditions—but could also encompass some genetic predisposing factors. Future studies will assist in identifying potential strategies to mitigate this risk.

The subsequent emergence of vancomycin resistance among enterococci in the mid-1980s and failure of such patients even if they had enterococci with vancomycin-intermediate susceptibility was described, resulting in vancomycin losing it omnipotence for all gram-positive cocci (12). The appearance of S. aureus strains with intermediate susceptibility to vancomycin (VISA) and vancomycin-resistant S. aureus (VRSA) (12–14) and vancomycin-resistant S. epidermidis (VRSE) (15, 16), brought an end to the hitherto hegemony of vancomycin in the Gram-positive coccal arena. Fortunately, the occurrence of these difficult to treat Staphylococci remains rare.

oral

toxicity

Vancomycin

Necrotizing Fasciitis (Streptococcal Gangrene): GAS necrotizing fasciitis is a rapidly progressing infection of the deep subcutaneous tissues and fascia with extensive and rapidly spreading necrosis. Infections often spare the skin, but 50% of patients may have associated myonecrosis. Necrotizing fasciitis is often associated with severe systemic involvement and an associated high mortality rate (7,80,87). As in other invasive streptococcal and staphylococcal skin infections, the site of inoculation is usually at area of minor trauma or the skin lesions of varicella. Like streptococcal bacteremia, there is a clear association between varicella and necrotizing fasciitis. Varicella is characterized by full-thickness dermal lesions that may induce selective immunosuppression to GAS, though this has not been substantiated (7). Necrotizing fasciitis caused by mixed infections, involving both aerobic and anaerobic Gram negative bacteria, is more likely to occur in the abdominal wall, following abdominal surgery or in diabetic patients.

antibiotic

Common symptoms are cellulites, swelling, redness, tenderness & discharge at the infected site, regional lymphadenopathy, chills, fever, high level of leukocyte & neutrophil.

High dose of penicillin is the common cure. As an alternative tetracycline & chloramphenicol is used in beta-lactam intolerant patients.

Isolation of Pasteurella multocida bacteria is usually done in sterile location such as the blood, pus or CSF.

culture