Clindamycin

Clindamycin is a semisynthetic derivative of lincomycin

Clindamycin has a bacteriostatic effect. It is a bacterial protein synthesis inhibitor by inhibiting ribosomal translocation, similar way to macrolides. 

Clindamycin may prolong the effects of neuromuscular-blocking drugs

Clindamycin is used primarily to treat anaerobic including dental, respiratory tract, skin, and soft tissue, and peritonitis. 

In hypersensitivity topenicillins, may be used to treat aerobicbacteria, in bone and joint, particular Staphylococcus aureus.

 Topical application of clindamycin phosphate can be used to treat mild to moderate acne.

It is most effective against infections involving the following types of organisms:

• Aerobic Gram-positive cocci, including some members of the Staphylococcus and Streptococcus (e.g. pneumococcus) genera, but not enterococci.
• Anaerobic, Gram-negative rod-shaped bacteria, including some Bacteroides, Fusobacterium, and Prevotella, although resistance is increasing in Bacteroides fragilis.

Most aerobic Gram-negative bacteria (such as Pseudomonas, Legionella, Haemophilus influenzae and Moraxella) are resistant to clindamycin, as are the facultative anaerobic Enterobacteriaceae. A notable exception is Capnocytophaga canimorsus, for which clindamycin is a first-line drug of choice.

Clindamycin may be useful in skin and soft tissue MRSA

Clindamycin is used in cases of suspected toxic shock syndrome, often in combination synergistically with a bactericidal agent such asvancomycin.  Both in vitro and in vivo studies have shown clindamycin reduces the production of exotoxins by staphylococci; it may also induce changes in the surface structure of bacteria that make them more sensitive to immune system attack (opsonization and phagocytosis).

Given with chloroquine or quinine, clindamycin is effective and well tolerated in treating Plasmodium falciparum malaria; the latter combination is particularly useful for children, and is the treatment of choice for pregnant women who become infected in areas where resistance to chloroquine is common

The combination of clindamycin and quinine is the standard treatment for severe babesiosis.

Clindamycin may also be used to treat toxoplasmosis,^[and, in combination with primaquine, is effective in treating mild to moderate Pneumocystis jirovecii pneumonia.

Common adverse drug reactions associated with clindamycin therapy — found in over 1% of patients — include: diarrhea,pseudomembranous colitis, nausea, vomiting, abdominal pain or cramps, rash, and/or itch. High doses (both intravenous and oral) may cause a metallic taste, and topical application may cause contact dermatitis.

Pseudomembranous colitis -Overgrowth of Clostridium difficile, which is inherently resistant to clindamycin

Rarely — in less than 0.1% of patients — clindamycin therapy has been associated with anaphylaxis, blood dyscrasias, polyarthritis,jaundice, raised liver enzyme levels, and/or hepatotoxicity.

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Antimotility agents are not indicated for infectious diarrhea, except for refractory cases of Cryptosporidium infection. Antimicrobial therapy is indicated for some nonviral diarrhea because most is self-limiting and does not require therapy.


Therapies recommended for some nonviral diarrheas include the following:

• Aeromonas species: Use cefixime and most third-generation and fourth-generation cephalosporins.
• Campylobacter species: Erythromycin shortens illness duration and shedding.
• C difficile: Discontinue potential causative antibiotics. If antibiotics cannot be stopped or this does not result in resolution, use oral metronidazole or vancomycin. Vancomycin is reserved for the child who is seriously ill.
• C perfringens: Do not treat with antibiotics.
• Cryptosporidium parvum: Administer paromomycin; however, effectiveness is not proven. Nitazoxanide, a newer anthelmintic, is effective against C parvum.
• Entamoeba histolytica: Metronidazole followed by iodoquinol or paromomycin is administered in symptomatic patients. Asymptomatic carriers in nonendemic areas should receive iodoquinol or paromomycin.
• E coli: Trimethoprim-sulfamethoxazole (TMP-SMX) should be administered if moderate or severe diarrhea is noted; antibiotic treatment may increase likelihood of hemolytic-uremic syndrome (HUS). Parenteral second-generation or third-generation cephalosporin is indicated for systemic complications.
• G lamblia: Metronidazole or nitazoxanide can be used.
• Plesiomonas species: Use TMP-SMX or any cephalosporin.
• Salmonella species: Treatment prolongs carrier state, is associated with relapse, and is not indicated for nontyphoid-uncomplicated diarrhea. Treat infants younger than 3 months and high-risk patients (eg, immunocompromised, sickle cell disease). TMP-SMX is first-line medication; however, resistance occurs. Use ceftriaxone and cefotaxime for invasive disease.
• Shigella species: Treatment shortens illness duration and shedding but does not prevent complications. TMP-SMX is first-line medication; however, resistance occurs. Cefixime, ceftriaxone, and cefotaxime are recommended for invasive disease.
• V cholerae: Treat infected individuals and contacts. Doxycycline is the first-line antibiotic, and erythromycin is second-line antibiotic.
• Yersinia species: TMP-SMX, cefixime, ceftriaxone, and cefotaxime are used. Treatment does not shorten disease duration; reserve for complicated cases.

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The following may be noted in patients with diarrhea:

• stool pH level of 5.5 or less or presence of reducing substances indicates carbohydrate intolerance, which is usually secondary to viral illness and transient in nature.
• Enteroinvasive infections of the large bowel cause leukocytes, predominantly neutrophils, to be shed into stool. Absence of fecal leukocytes does not eliminate the possibility of enteroinvasive organisms. However, presence of fecal leukocytes eliminates consideration of enterotoxigenic E coli, Vibrio species, and viruses.
• Examine any exudates found in stool for leukocytes. Such exudates highly suggest colitis (80% positive predictive value). Colitis can be infectious, allergic, or part of inflammatory bowel disease (Crohn disease, ulcerative colitis).
• Always culture stool for Salmonella, Shigella, and Campylobacter organisms and Y enterocolitica in the presence of clinical signs of colitis or if fecal leucocytes are found.
• Look for C difficile in persons with episodes of diarrhea characterized by colitis and/or blood in the stools. Remember that acute-onset diarrheal episodes associated with C difficile may also occur without a history of antibiotic use.
• Bloody diarrhea with a history of ground beef ingestion must raise suspicion for enterohemorrhagic E coli. If E coli is found in the stool, determine if the type of E coli is O157:H7. This type of E coli is the most common, but not only, cause of HUS.
• History of raw seafood ingestion or foreign travel should prompt additional screening for Vibrio and Plesiomonas species.
  
  
  Other laboratory studies may include the following:
  

  • Serum albumin levels: Low in protein-losing enteropathies from enteroinvasive intestinal infections (eg, Salmonella spp, enteroinvasive E coli)
  • Fecal alpha1-antitrypsin levels: High in enteroinvasive intestinal infections
  • Anion gap to determine nature of the diarrhea (ie, osmolar vs secretory)
  • Intestinal biopsy: May be indicated in the presence of chronic or protracted diarrhea, as well as in cases in which a search for a cause is believed to be mandatory (eg, in patients with acquired immunodeficiency syndrome [AIDS] or patients who are otherwise severely immunocompromised)
    
     Because the pathogenesis of diarrhea can be either osmolar (due to the presence of an excess of unabsorbed substrates in the gut lumen) or secretory (due to active anion secretion from the enterocytes), the anion gap in the stools is occasionally used to ascertain the nature of the diarrhea. The stool anion gap is calculated according to the formula: 290 - [(Na+K) X 2]. If the value is more than 100, osmolar diarrhea can be assumed to be present. If the value is less than 100, the diarrhea has a secretory origin.

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