they were not resistant to ciprofloxacin in patients with pneumonia (P = 0.016).

We and other authors have reported a high prevalence of hypermutable H. influenzae isolates causing respiratory infections (22, 24). We also noticed a high rate of fluoroquinolone resistance in these isolates (22) and reported a therapeutic failure in a community-acquired pneumonia case due to levofloxacin-resistant H. influenzae (2).

1.7 cases per 100,000 children younger than 5 years of age and 5.0 cases per 100,000 adults 65 years of age or older

Patients ≥65 years of age with invasive H. influenzae disease (Hib, non-b, and nontypeable) have higher case-fatality ratios than children and young adults.

The oxidase test is used to identify bacteria that produce cytochrome c oxidase, an enzyme of the bacterial electron transport chain.

Additionally, Hap mediates adherence to fibronectin, laminin and collagen IV, extracellular matrix (ECM) proteins that are present in the respiratory tract and are probably important targets for H. influenzae colonization.

SIGNS AND SYMPTOMSIn

The IgA protease, showing its teeth in red!An Arms RaceSome bacteria have developed weapons that can cut our antibodies into small pieces so that they become unable to stick the invading bacteria into clumps. These anti-antibodies are called IgA proteases and are produced inside bacteria like the ones that cause meningitis and gonorrhoea

By blocking this protein enzyme it stops the release of viruses from the infected host cell and prevents new host cells from being infected.

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.

Nosocomial outbreaks of infection due to non-typeable Haemophilus influenzae (NTHi) are rarely described. There are a few published reports that suggest that elderly patients with underlying pulmonary disease are at risk and that person-to-person spread is key to disease transmission. During the summer months of 2005, we documented an outbreak of NTHi infections in a Veterans Affairs nursing home. Thirteen patients developed conjunctivitis or lower respiratory infection involving a beta-lactamase-negative biotype III NTHi isolate, with an indistinguishable SmaI macrorestriction pattern. Patients were elderly males usually with underlying cardiac and pulmonary disease.

Table 2

the United States down from 36% in 1994 to 26% in 2002

overall prevalence of 16.6% β-lactamase-positive strains, ranging from as low as 3% in Germany to as high as 65% in South Korea

Its capsule, the adhesion proteins, pili, the outer membrane proteins, the IgA1 protease and, last but not least, the lipooligosaccharide,

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

Oral antibiotics such as β-lactams are appropriate first-line therapy for most patients. A proportion of H. influenzae isolates produce β-lactamase (this varies markedly between different locations) and in this circumstance, extended spectrum cephalosporins, amoxicillin-clavulinic acid, trimethoprim-sulfamethoxazole, tetracyclines, quinolones and macrolide antibiotics are appropriate therapeutic choices.

Evasion of mucosal immunity

Their capsule allows them to resist phagocytosis and complement-mediated lysis in the nonimmune host.

The organism enters the body through the nasopharynx. Organisms colonize the nasopharynx and may remain only transiently or for several months in the absence of symptoms (asymptomatic carrier).

Cephalosporins are bactericidal (kill bacteria) and work in a similar way to penicillins. They bind to and block the activity of enzymes responsible for making peptidoglycan, an important component of the bacterial cell wall. They are called broad-spectrum antibiotics because they are effective against a wide range of bacteria.

Amoxicillin/clavulanate

The third generation cephalosporins have a marked activity against gram-negative bacteria due to enhanced beta-lactamase stability and the ability to penetrate the gram-negative cell wall. They have more favorable pharmacologic properties than previous generations.

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

Haemophilus influenzae type b bacteria can’t survive on surfaces or in the environment. The bacterium’s only known reservoir is humans, who may carry it without becoming ill.

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

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

Laboratory testing Gram staining of body fluids from various sites of infection Bacterial culture (blood, other body fluids): The most confirmatory method of establishing the diagnosis; slide agglutination with type-specific antisera is used for serotyping H influenzae Immunologic studies: Detection of the polyribosyl ribitol phosphate (PRP) polysaccharide capsule via countercurrent immunoelectrophoresis, latex particle agglutination, co-agglutination, and enzyme-linked immunosorbent assay; important adjuncts to culturing for rapid diagnosis Cerebrospinal fluid (CSF) studies (eg, Gram stain, culture, glucose/protein levels) Blood cell counts: Assessment for anemia, leukocytosis, thrombocytosis, and/or thrombocytopenia Acute phase reactants: Characteristic elevated erythrocyte sedimentation rates (ESRs) and C-reactive protein (CRP) levels in patients with septic arthritis

Haemophilus influenzae is a small (1 µm × 0.3 µm), pleomorphic, gram-negative coccobacillus.

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.

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

Biochemical Tests

On Blood Agar: translucent, low, convex or flat pin point colonies, Satellitism. On Chocolate Agar: Grayish, Transparent, smooth, low, convex or flat with a slightly splayed out, entire edge, mucoid, pale

Slender, short, gram negative rods or coccobacillus 3-0.5 um X 0.5-1 um with rounded ends.

Haemophilus influenzae infection is transmitted by droplets from infected (but not necessarily symptomatic) people. Haemophilus influenzae type b be can be prevented by vaccination.

Haemophilus influenzae type b is a Gram-negative bacterium that causes meningitis and acute respiratory infections, mainly in children