Some clinical aspects of diarrheal diseases;
-Enteropathogenic E. coli (EPEC) are an important cause of diarrhea in infants, especially in developing countries. EPEC previously was associated with outbreaks of diarrhea in nurseries in developed countries. EPEC adhere to the mucosal cells of the small bowel. Based on their characteristic lesions they are seen on electron micrographs of small bowel biopsy lesions. The result of EPEC infection in infants is severe, watery diarrhea; vomiting; and fever, which is usually self-limited but can be prolonged or chronic.

– Enterotoxigenic E.coli (ETEC) is a common cause of “traveler’s diarrhea” and a very important cause of diarrhea in infants in developing countries. ETEC colonization factors (known as colonization factor antigens CFAs) specific for humans promote adherence of ETEC to epithelial cells of the small bowel. Some strains of ETEC produce a heat-labile exo-toxin (LT) (molecular weight MW, 80,000) that is under the genetic control of a plasmid. Care in the selection and consumption of foods potentially contaminated with ETEC is highly recommended to help prevent traveler’s diarrhea. Antimicrobial prophylaxis can be effective but may result in increased antibiotic resistance in the bacteria and probably should not be uniformly recommended. When diarrhea develops, antibiotic treatment effectively shortens the duration of disease.
-Entero-invasive E. coli (EIEC) produces a disease very similar to shigellosis. The disease occurs most commonly in children in developing countries and in travelers to these countries. Similar to Shigella, EIEC strains are nonlactose or late lactose fermenters and are nonmotile. EIEC produce disease by invading intestinal mucosal epithelial cells.
-Entero-aggregative E. coli (EAEC) causes acute and chronic diarrhea (>14 days in duration) in persons in developing countries. These organisms also are the cause of food-borne illnesses in industrialized countries and have been associated with traveler’s diarrhea and persistent diarrhea in patients with HIV. They are characterized by their specific patterns of adherence to human cells. This group of diarrhea-genic E. coli is quite heterogeneous, and the exact pathogenic mechanisms are still not completely elucidated. Some strains of EAEC produce ST-like toxin , others produces a plasmid-encoded enterotoxin that produces cellular damage. Diagnosis can be suspected clinically but requires confirmation by tissue culture adhesion assays not readily available in most clinical laboratories.
3. Sepsis
Sepsis occurs when normal host defenses are inadequate, E coli may reach the bloodstream and cause sepsis. Newborns may be highly susceptible to E coli sepsis because they lack IgM anti-bodies. Sepsis may occur secondary to urinary tract infection.
3. Meningitis
E coli and group B streptococci are the leading causes of meningitis in especially in infants. Approximately 75% of E. coli from meningitis cases have the K1 antigen. This antigen cross-reacts with the group B capsular polysaccharide of N meningitides. The mechanism of virulence associated with the K1 antigen is not understood.

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Symptoms of P. aerugenosa vary based on the type of infection.
Bloodstream infections can cause various symptoms, including:
• Fever
• Body aches
• Light-headedness
• Diarrhea
• Decrease urination
• Rapid pulse and breathing.
Pneumonia can cause:
• Difficulty in breathing
• Fever and chills
• cough, sometimes with yellow, green, or bloody mucus

Urinary tract infection can cause:
• Strong urge to urinate frequently
• Painful urination
• Unpleasant odor in urine
• Cloudy or bloody urine
Wound infection can cause:
• Inflamed wound site
• Fluid leakage from wound
Ear infection can cause:
• Ear pain
• Dizziness and disorientation
• Hearing loss

Significant infections with P. aeruginosa have not been treated with single-drug therapy traditionally because the success rate is low with such therapy and the bacteria can rapidly develop resistance when single drugs are used. An extended spectrum penicillin such as piperacillin active against P .aeruginosa is used in combination with an aminoglycoside, usually tobramycin. Other drugs active against P. aeruginosa include aztreonam; carbapenems such as imipenem or meropenem; and the fluoroquinolones, including ciprofloxacin. Of the cephalosporins, ceftazidime, cefoperazone, and cefepime are active against P aeruginosa; ceftazidime is often used with an aminoglycoside in primary therapy of P .aeruginosa infections, especially in patients with neutropenia.
The susceptibility patterns of P aeruginosa vary geographically, and susceptibility tests should be done as an adjunct to selection of antimicrobial therapy. Multidrug resistance has become a major issue in the management of hospital-acquired infections with P aeruginosa because of acquisition of chromosomal ?-lactamases, extended-spectrum ?-lactamases, porin channel mutations, and efflux pumps. (Henry et al., 2011).
The sulfonamides, ampicillin, cephalosporins, fluoroquinolones, and aminogly-cosides have marked antibacterial effects against the enterics, but variation in susceptibility is great, and laboratory tests for antibiotic susceptibility are essential. Multiple drug resistance is common and is under the control of transmissible plasmids. Certain conditions predisposing to infection by these organisms require surgical correction, such as relief of urinary tract obstruction, closure of a perforation in an abdominal organ, or resection of a bronchiectatic portion of lung. Treatment of gram-negative bacteremia and impending septic shock requires rapid institution of antimicrobial therapy, restoration of fluid and electrolyte balance, and treatment of disseminated intravascular coagulation. Various means have been proposed for the prevention of traveler’s diarrhea, including daily ingestion of bismuth sub-salicylate suspension (bismuth subsalicylate can inactivate E coli enterotoxin in vitro) and regular doses of tetracycline or other antimicrobial drugs for limited periods. Because none of these methods are entirely successful or lacking in adverse effects, it is widely recommended that caution be observed in regard to food and drink in areas where environmental sanitation is poor and that early and brief treatment (eg, with ciprofloxacin or trimethoprim–sulfamethoxazole) be substituted for prophylaxis.( Naataro et al., 2011).