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

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,

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 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

Historically, the relative proportion of bacterial agents in AOM was Streptococcus pneumoniae at 40%, Haemophilus influenzae at 25% and Moraxella catarrhalis at 12%.

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.

Klebsiella Infections Medication

Clinical Infectious DiseasesIDSAGUIDELINEManagement of Adults With Hospital-acquired andVentilator-associated Pneumonia: 2016 Clinical PracticeGuidelines by the Infectious Diseases Society of Americaand the American Thoracic Society

Infectious Diseases Society of America/AmericanThoracic Society Consensus Guidelines on theManagement of Community-Acquired Pneumoniain Adults

Empiric treament of severe nosocomial infections in critically ill patients or in ICU

Effective therapy for severe community acquired K. pneumoniae pneumonia consists of empiric treatment with coverage against Gram negative organisms, aggressive ventilation, and clinical and radiologic surveillance for surgically treatable entities such as pulmonary gangrene, lung abscess and empyema (111, 141, 180). Third generation cephalosporins or quinolones would provide coverage against most community acquired K. pneumoniae. Macrolides (including azithromycin) have no useful activity against K. pneumoniae. The superiority of combinations of third generation cephalosporins and aminoglycosides has been demonstrated in one study (111) but not in others (129, 131). The clinical outcome when chloramphenicol and aminoglycosides are used in combination has been poor (118).

Critically ill patients with nosocomial Klebsiella bacteremia should probably be treated with antibiotics active against ESBL producers until the absence of an ESBL is definitively established.

Selection of antimicrobial therapy for Klebsiella bacteremia should be based on local susceptibility patterns of isolates causing bacteremia. In particular, the likelihood that an isolate may be an ESBL producer is an important consideration.

All isolates were sensitive to vancomycin, ofloxacin, ampicillin, ciprofloxacin, nitrofurantoin and penicillin. However, the following number of clinical isolates exhibited intermediate or decreased sensitivity, nine (17%) to ampicillin, eight (15%) to penicillin, 14 (32%) to ciprofloxacin and one (2%) to nitrofurantoin. Thirty-one percent of the isolates were resistant to azithromycin and ceftriaxone, 19% to clindamycin, 15% to cefazolin and 13% to cefamandole. Eighteen (35%) of the clinical isolates tested were resistant to 6 of the 12 antibiotics tested.

The proportions of GBS isolates with in vitro resistance to clindamycin or erythromycin have increased over the past 20 years. The prevalence of resistance among invasive GBS isolates in the United States ranged from 25% to 32% for erythromycin and from 13% to 20% for clindamycin in reports published during 2006–2009 (19,106,108).

Vancomycin-associated nephrotoxicity can still be seen, even in the presence of appropriate serum concentrations, especially when it is co-administered with aminoglycosides, amphotericin B, foscarnet, pentamidine ACE inhibitors, loop diuretics, cyclosporine, cyclophosphamide

it is likely remain effective as long as resistance to vancomycin remains controlled.

Humans (neonates, elderly, immunocompromised, diabetic, alcoholic, and stroke and cancer patients have a higher risk of infection), cattle (mastitis), dogs, cats, rabbits, horses, guinea pigs, and goats have been shown to contain the infectious agent

Laboratory Photo Examples

Antibiotics used to treat tularemia include streptomycin, gentamicin, doxycycline, and ciprofloxacin.

likely exposures, such as tick and deer fly bites, or contact with sick or dead animals. 

This is the most serious form of tularemia. Symptoms include cough, chest pain, and difficulty breathing. This form results from breathing dusts or aerosols containing the organism.

All forms are accompanied by fever, which can be as high as 104 °F

All forms are accompanied by fever, which can be as high as 104 °F.

Growth of F. tularensis in culture is the definitive means of confirming the diagnosis of tularemia. Appropriate specimens include swabs or scrapings of skin lesions, lymph node aspirates or biopsies, pharyngeal swabs, sputum specimens, or gastric aspirates, depending on the form of illness.

and not just through person-to-person contact --