Next, the Lassa virus enters to the inside of the cell by receptor-mediated endocytosis [5].

The pathogen enters a person through the fecal-oral route

It does this by first being endocytosed and then fusing its envelope with the plasma membrane of the target cell

SARS may be spread via fecal-oral contamination (Stark, 2005)

Enterobacter species account for a small fraction of postsurgical endophthalmitis and posttraumatic cases. [18] Most ophthalmic infections are caused by gram-positive organisms, but Enterobacter species and Pseudomonas species are among the most aggressive pathogens.

Enterobacter cloacaeATCC 13047 Growth good to excellent; colonies medium-sized, deep blue, with or without violet halos

Characteristics   E. coli

The symptoms of STEC infections vary for each person but often include severe stomach cramps, diarrhea (often bloody), and vomiting. If there is fever, it usually is not very high (less than 101˚F/less than 38.5˚C). Most people get better within 5–7 days. Some infections are very mild, but others are severe or even life-threatening.

Some kinds of E. coli cause disease by making a toxin called Shiga toxin. The bacteria that make these toxins are called “Shiga toxin-producing” E. coli, or STEC for short. You might hear these bacteria called verocytotoxic E. coli (VTEC) or enterohemorrhagic E. coli (EHEC); these all refer generally to the same group of bacteria

People mainly become infected with EHEC O157:H7 by ingesting contaminated food and water, or during contact with animals(especially ruminants), feces and contaminated soil. The infectious dose for humans is estimated to be less than 100 organisms, and might be as few as 10.Foodborne outbreaks caused by EHEC O157:H7 are often associated withundercooked or unpasteurized animal products, particularly ground beef,but alsoother meats and sausages(e.g., roast pork, salami, venison)and unpasteurized milk and cheese.Additionaloutbreaks have been linked to lettuce, spinach,various sproutsand other contaminated vegetables, unpasteurized cider, nuts and even pickled vegetables. Contaminated irrigation water is an important source of EHEC O157:H7 on vegetables.

Person-to-person transmission of EHEC and EAHEC can contribute to disease spread during outbreaks, via the fecal-oral route.

bacterial attachment to the epithelial cell membrane and the destruction of microvilli at the site of adherence.

Most EHEC carry virulence factors (such as the intimin gene, eae) that give them the ability to cause attaching and effacing (A/E) lesions on human intestinal epithelium.

Escherichia coliis a Gram negative rod (bacillus) in the family Enterobacteriaceae. Most E. coliare normal commensals found in the intestinal tract.

Intimin, an out membrane protein expressed by EHEC and EPEC, is required for intimate attachment to the host cell and formation of the A/E lesions [17]. Tir is a bacterial protein which injects into the host cell through the Type III secretion system (T3SS) to function as a receptor specific to intimin[17], [18]. The binding of intimin to Tir mediates the adhesion between the pathogen and its host cell[19]. Shortly after the successful binding, the translocated Tir protein triggers additional signal transduction and actin polarization in host cells, which are essential for lesion formation

The H. influenzae Hap autotransporter is a non-pilus adhesin that promotes adherence to epithelial cells and selected extracellular matrix proteins and mediates bacterial aggregation and microcolony formation. In addition, Hap has serine protease activity.

Selected human mucosal pathogens express immunoglobulin (Ig) A proteases, which are strongly associated with virulence. IgA proteases are a striking example of convergent evolution because 3 independent lines of these highly specific postproline endopeptidases (serine, metallo-, and cysteine types) are present in human bacterial pathogens, indicating a key role for IgA proteases in the host-pathogen interaction [1–3]. Discovered 30 years ago, IgA proteases cleave the hinge region of human IgA1, dissociating its antigen-binding Fab domains from the Fc domain, thus inhibiting functions of IgA, such as agglutination, inhibition of bacterial adhesion to epithelial cells, and opsonization

Lipooligosaccharide (LOS) is the major immunogen on the H. influenzae surface and features an assortment of short (<15 saccharide units) oligosaccharides extending from all three heptoses of a triheptose core region (33). These oligosaccharides contain a number of molecules which mimic host structures, such as human blood-group antigens containing sialic acid and phosphorylcholine (ChoP) (25, 26, 35-37). The expression of host structures within the LOS has been proposed to be a means for utilizing host receptors to facilitate colonization

In addition to buccal epithelial cells, pili also mediateadherence to bronchial epithelial cells (25)

Worldwide, H. influenzae is the second commonest bacterial pathogen in community acquired pneumonia (237). Non-typeable H. influenzae strains cause most H. influenzae pneumonia, especially in the elderly and in those with chronic respiratory diseases such as acute exacerbations of chronic bronchitis, cystic fibrosis and bronchiectasis. 

A polysaccharide capsule has been shown to confer tolerance to trimethoprim-sulfamethoxazole for some H. influenzae type b. That is they have a high MBC of > 4/76 µg/ml but a low MIC of <0.03/0.6 µg/ml. One consequence is that a proportion of H. influenzae type b with virulence potential may persist in the nasopharynx of carriers after trimethoprim-sulfamethoxazole therapy whereas relatively benign non-typeable H. influenzae strains may be eradicated

Table 2: Susceptibility of Worldwide Isolates of H. influenzae (n=8,523) to 23 Antimicrobials and MIC50s and MIC90sa

H. influenzae appear as large, round, smooth, convex, colorless-to-grey, opaque colonies on a CAP

H. influenzae is a fastidious organism which grows best at 35-37°C with ~5% CO2 (or in a candle-jar) and requires hemin (X factor) and nicotinamide-adenine-dinucleotide (NAD, also known as V factor) for growth. The standard medium used for growth of H. influenzae is a chocolate agar plate (CAP), which can be prepared with heat-lysed horse blood, a good source of both hemin and NAD, although sheep blood can also be used.

Figure 1. H. influenzae colonies on a CAP

Fever and chills Cough Shortness of breath or difficulty breathing Sweating Chest pain Headache Muscle pain or aches Excessive tiredness

These bacteria live in the nose and throat, and usually cause no harm. However, the bacteria can sometimes move to other parts of the body and cause infection.