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1. Institute of Biomedical Sciences Unit of Microbiology and Immunology GASTROINTESTINAL SYSTEM MODULE -5

2. Infections of The O ral C avity and Esophagus After this session student will be able :- To discuss microbial pathogens that infected oral cavity and esophagus To discuss the source and route of transmission, pathogenesis, diagnosis, treatment and control and prevention of oral cavity and esophagus To discuss cause and pathogenesis of dental caries

3. Oral cavity infections The mouth is the gateway of the body to the external world and represents one of the most biologically complex and significant sites in the body. This is where the first stages of the digestive process take place Mouse can act as a site of entry for some microbial pathogens, especially from the air or via ingestion from the diet.

4. Infection of oral cavity The oral cavity contains some of the most varied and vast flora in the entire human body Oral cavity are the main entrance for two systems vital to human function and physiology. i.e The gastrointestinal and respiratory systems There are several causative agents can involved in oral infection such as bacterial organisms, oral microorganisms can include fungal, protozoal, and viral species. A variety of organisms in the microenvironment of the oral cavity adhere to the teeth, the gingival sulcus, the tongue, and the buccal mucosa

5. Distribution of the microflora at distinct sites in the mouth

6. The mouth is similar to other sites in the body in having a natural microflora in a harmonious relationship with the host But the relationship between mouth and microflora( microenvironment of the oral cavity) can be break m ajor changes to the biology of the mouth from exogenous sources (examples include: antibiotic treatment or the frequent intake of fermentable carbohydrates in the diet) or f rom endogenous changes such as alterations in the integrity of the host defences following drug therapy, T he presence of microorganisms at sites not normally accessible to them; for example, when oral bacteria enter the blood stream following tooth extraction or other traumas and are disseminated to distant organs, where they can cause abscesses or endocarditis

7. Other possible factors; the age of the patient , and the appearance of disease states Systemic changes, such as pregnancy or drug intake , also alter the number and proportion of flora These changes are due to alterations in the flow and composition of salivary fluid and in the levels and activity of defense components ( e.g , immunoglobulins , cytokines) in the saliva.

8. INFECTIONS OF THE ORAL CAVITY AND ESOPHAGUS

9. WHAT IS Gingivitis? The term Gingivitis is used when the inflammatory condition is limited to the marginal gingiva and bone resorption around the necks of teeth has not yet begun. Gingivitis is inflammation of the gingival tissue . Gingivitis is characterized by areas of redness and swelling, and there is a tendency for the gingiva to bleed easily . Gingivitis is limited to the epithelium and gingival connective tissues . It is important to note that there is no tissue recession or loss of connective tissue or bone

10. Cont.. The simplest form of gingivitis is associated with the accumulation of supragingival plaque along the gingival margins of the teeth The initial colonizers of the teeth are streptococci, which proliferate and in turn become colonized by other bacteria present in saliva, such as various Actinomyces species and Veillonella The greatest growth of the plaque occurs at the gingival margin, where plaque accumulations usually are visible after several days

11. Dental plaque is a general term for the complex microbial community that develops on the tooth surface, embedded in a matrix of polymers of bacterial and salivary origin. The presence of plaque in the mouth can readily be demonstrated by rinsing with a disclosing solution such as erythrosin (Fig. 5.1). The majority of plaque is found associated with the protected and stagnant regions of the tooth surface such as fissures, approximal regions between teeth, and the gingival crevice (see Fig. 5.1). Plaque is found naturally on the tooth surface, and forms part of the host defences by excluding exogenous (and often pathogenic) species ( colonization resistance ) On occasions, however, plaque can accumulate beyond levels compatible with oral health, and this can lead to shifts in the composition of the microflora and predispose sites to disease

12. Cont … This plaque may, in some instances, provoke a bleeding gingivitis in which spirochetes and Actinomyces viscosus are prominent members of the plaque flora. Gingivitis is extremely common, and is manifested clinically as bleeding of the gingival or gum tissues without evidence of bone loss or deep periodontal pockets

13. Cont.. If this plaque remains undisturbed, the flora gradually shifts toward an anaerobic, Gram negative flora that includes black pigmented bacteroides and several types of spirochetes. The increase in these anaerobic organisms can be explained by the low oxidation reduction potential of the aged plaque and by nutrients derived from the inflammatory exudate at the site.

14. Classification according to Course 1. ACUTE GINGIVITIS : – It is of sudden onset and short duration and can be painful . – A less severe form of acute condition is called SUBACUTE. 2. RECURRENT GINGIVITIS : – Reappears after eliminated by treatment or disappearing spontaneously . 1. CHRONIC GINGIVITIS : – Slow in onset and of long duration, and is painless, inflammation persists or resolves and normal areas become inflamed.

15. S. mitus S. oralis S. sanguis Streptococcus sp. S. intermedius Subgingival Microbial Complex P. intermedia F. nuc . nucleatum F. nuc . vincentil F. nuc . polymorphum F. periodonticum P. gingivalis Treponema spp E. corrodens C. gingivalis C. sputigena C. ochracea C. concisus Actinomyces species E. nodatum

16. Herpes Simplex Viruses Symptoms include fever, sore throat, vesicular and ulcerative lesions, gingivostomatitis, and malaise Gingivitis (swollen, tender gums) is the most striking and common lesion . 21 Clinical Findings

17. Herpes simplex gingivostomatitis 22

18. HSV Recurrent herpes labialis is the most frequent clinical manifestation of reactivation most commonly seen in children and young adults Cluster of vesicles most commonly localized at the border of the lip Intense pain that fades over 4–5 days. Fever, malaise, myalgias , inability to eat, irritability, and cervical adenopathy , may last from 3 to 14 days 23

19. Herpes Simplex Viruses 24 Figure Recurrent herpes simplex labialis Recurrent herpes simplex virus vesicles on the mucocutaneous margin of the lip. Clinical Findings

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21. The main function of the periodontium is to attach the tooth to the bone tissues of the jaws and to maintain integrity of the surface of the masticatory mucosa of the oral cavity Definition Periodontal disease can establish itself when the gums detach from the teeth as a result of an inflammatory response to plaque Etiology Periodontal infections are usually mixed, most often involving anaerobes such as Treponema denticola and Porphyromonas gingivalis . The microaerophile Actinobacillus actinomycetemcomitans causes a rare form known as localized juvenile periodontitis 28

22. Pathogenesis Plaque bacteria elaborate various compounds (H2S, NH3, amines, toxins, enzymes, antigens , etc.) that elicit an inflammatory response that is protective but also is responsible for loss of periodontal tissue, pocket formation, and loosening and loss of teeth . Clinical Manifestations There is no apparent pain until very late when abscesses may occur. Bleeding gums and bad breath may occur. 29

23. Microbiologic Diagnosis Microbiologic diagnosis is usually not sought. Spirochetes and other motile organisms are found upon dark-field microscopic examination. Immunologic reagents, DNA probes and enzyme assays have been developed for P gingivalis , T denticola , Bacteroides forsythus , A actinomycetemcomitans and other organisms. 30

24. Prevention and Treatment Daily tooth brushing and regular professional cleanings by the dentist appear to be adequate to prevent periodontal disease. Rigorous debridement of tooth surfaces is the standard treatment. Often, some form of surgery is used to improve access to root surfaces . Recent studies suggest that short-term use of antimicrobial agents, especially metronidazole and doxycycline, is beneficial. 31

25. Periodontal disease Periodontal disease is an infectious disease process that involves inflammation. Periodontal diseases involve the structures of the periodontium. Periodontal disease can cause a breakdown of the periodontium resulting in loss of tissue attachment and destruction of the alveolar bone. 32

26. Periodontal disease is the general description applied to the inflammatory response of the gingiva and surrounding connective tissue to the bacterial or plaque accumulations on the teeth . Periodontal diseases range from simple gum inflammation to serious disease that results in major damage to the soft tissue and bone that support the teeth 33

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28. Gingivitis  Early stage of disease  Red, swollen, and bleeding gums  Usually reversible through good oral hygiene and preventive care  Not uncommon in young adults and even youth  Periodontitis  Advanced stage of disease  Chronic inflammatory response leading to irreversible destruction of tissues and bone that support the teeth  Treatment requires more aggressive surgical care 35

29. Periodontal diseases are the leading cause of tooth loss in adults. Almost 75% of American adults have some form of periodontal disease, and most are unaware of the condition. Almost all adults and many children have calculus on their teeth. Fortunately, with the early detection and treatment of periodontal disease, most people can keep their teeth for life.

30. Systemic Conditions: Links to Periodontal Disease Certain systemic conditions increase the patient’s susceptibility to periodontal disease, and periodontal disease may actually increase a patient’s susceptibility to certain systemic conditions. Cardiovascular disease Preterm low birthweight Respiratory disease

31. Examples are Capnocytophaga species and Rothia dentocariosa . Capnocytophaga species are fusiform , gram-negative, gliding anaerobes; Rothia species are pleomorphic, aerobic, gram-positive rods. Both probably participate in the complex microbial flora of periodontal disease with prominent bone destruction In granulocytopenic immunodeficient patients, they can lead to serious opportunistic lesions in other organs

32. Buildup of bacterial plaque on the teeth affects the gingival tissues

33. Copyright © 2005 by Elsevier Inc. All rights reserved. Signs and Symptoms of Periodontal Disease Red, swollen, or tender gingiva Bleeding gingiva while brushing or flossing Loose or separating teeth Pain or pressure when chewing Pus around the teeth or gingiva

34. Etiology and Pathogenesis These infections are unusual in that massive or even obvious bacterial invasion of the tissues is rarely encountered Rather, bacteria in the plaque touching the tissue elaborate various compounds, such as H2S, NH3 , amines, endotoxins, enzymes (such as collagenases) and antigens, all of which penetrate the gingiva and elicit an inflammatory response

35. This inflammatory response although overwhelmingly protective, appears to be responsible for a net loss of periodontal supporting tissue, and leads to periodontal pocket formation, loosening of the teeth , and eventual tooth loss N eutrophils are extremely important in this inflammatory response and, if they are absent, as in various N eutropenias , or compromised as a result of chemotherapy, an aggressive form of periodontitis is encountered. T4 helper cells play a role in this defense of perodenitis.

36. Localized Juvenile Periodontitis (LJP) LJP is different from all other periodontal infections, as it is not associated with plaque accumulations or calculus , is localized to certain anterior or front teeth and first molars , and is seen following puberty Bacterial examinations of subgingival plaque from affected teeth and adjacent healthy teeth, revealed that the diseased teeth were colonized by an essentially Gram-negative flora dominated by organisms subsequently identified as various Capnocytophaga and Wolinella species and Actinobacillus actinomycetemcomitans Once LJP has been recognized clinically, most of the tissue damage has already occurred, thereby permitting only a retrospective diagnosis of an A actinomycetemcomitans infection .

37. A actinomycetemcomitans is found at a higher prevalence in tooth sites associated with LJP and at a lower prevalence in healthy sites in the same mouth, or at sites in periodontally healthy individuals. A actinomycetemcomitans produces a leukotoxin that kills neutrophils in vitro

38. Early-Onset Periodontitis (EOP) and Adult Periodontitis (AP) The more common forms of periodontitis comprise at least two clinical entities, an early onset form in mainly young individuals and a chronic form seen in older adults . The early-onset periodontitis (EOP) is more aggressive looking, while the adult periodontitis (AP ) may reflect a stable, but tenuous, stand-off between the host's defensive systems and the plaque bacteria It is not clear whether these entities represent multiple types of infections with two clinical manifestations, or a single mixed anaerobic infection with different levels of host containmen

39. The inability to distinguish microbiologically between these two general patterns reflects methodologic procedures relating to the sampling of the subgingival plaque For example, the spirochetes cannot be quantitatively cultured and may account for more than 40% of the flora in EOP and AP O ne of these cultivable species predominates in all disease-associated plaques. For example, Bacteroides forsythus , a nonpigmenting fusiform organism has been associated with the active periodontal lesion. B forsythus is present in 13% of the active sites and at 8% of the inactive sites, a difference which is hardly indicative of etiologic association

40. It has been shown to possess a wide array of enzymes, such as a collagenase , peptidases, hyaluronidase , and a keratinolytic enzyme, and to produce noxious end products, such as butyrate, NH3, H2S, and endotoxin, that could cause, if they entered the periodontal tissue, an inflammatory response. However , comparable enzymes occur in P gingivalis and other anaerobic species found in the plaque, so that it would be difficult to assign etiologic significance to any one of these organisms based on the production of these enzymes.

41. Clinical Manifestations Periodontal disease is usually painless until late in the disease process, when the teeth are so loose that some discomfort may appear upon chewing Retention of food in a pocket site may provoke a sudden burst of microbial growth which could result in a painful abscess At other times, the anterior teeth may become so loose that they separate and the patient visits a dentist because of the resulting poor aesthetics

42. Prevention and Treatment Gingivitis can be prevented by good oral hygiene and professional surveillance . Gingivitis can be effectively treated by debridement of the teeth, and, if needed, by short term use of products containing chlorhexidine , stannous fluoride, or other antimicrobial agents . Mouth rinses, gels, and toothpastes, when used in conjunction with toothbrushing and flossing, are probably adequate to deliver any antimicrobial agents to subgingival sites that are 1 to 3 mm in depth Clinical dentistry has been about 80 to 85% successful in treating periodontitis by debridement and surgical procedures. .

43. A actinomycetemcomitans is sensitive to tetracycline, and early uncontrolled studies showed that tetracycline, scaling and root planing , periodontal flap surgery, and topical treatment with chlorhexidine were able, to save hopeless teeth in LJP patients

44. Dental Caries (Decay) Dental caries is the progressive destruction of the mineralized tissues of the tooth, primarily caused by the production of organic acids( derived from bacterial fermentation of sucrose and other dietary carbohydrates) resulting from the glycolytic metabolic activity of plaque bacteria T he basic characteristic of the carious lesion is that it progresses inward from the tooth surface, either the enamel-coated crown or the cementum of the exposed root surface, involving the dentin and finally the pulp of the tooth From there, infection can extend out into the periodontal tissues at the root apex or apices

45. Dental plaque is a soft, adherent dental deposit that forms as a result of bacterial colonization of the tooth surface . It is rather insoluble, as well as adherent, and thus resists removal by water spray or mouth rinsing. Only more vigorous means such as tooth brushing and flossing between the teeth remove it. It consists almost entirely of bacterial cells (1.7 1011 cells/g wet weight). These bacteria live in bacterial communities known as dental plaque which accumulates on the tooth surface.

46. Dental Caries is a disintegration of the teeth beginning at the surface and progressing inward. First the surface enamel, which is entirely noncellular, is demineralized. This has been attributed to the effect of acid products of glycolytic metabolic activity when the plaque bacteria are fed the right substrate . Subsequent decomposition of the dentin and cementum of the exposed root surface involves bacterial digestion of the protein matrix.

47. Four major factors involved in etiology:- • Cariogenic bacteria • Bacterial plaque • Susceptible tooth surface • Fermentable bacterial substrate (sugar)

48. Dental caries.. S mutans is considered to be the dominant organism for the initiation of caries; however, multiple members of the plaque biofilm participate in the evolution of the lesions . These include other streptococci ( S salivarius , S sanguis , S sobrinu s ), lactobacill i ( L acidophilus, L casei ), and actinomycetes (A viscosis , A naeslundii ). The large amounts of organic acid products produced from carbohydrates by the interaction of S mutans with these other species in plaque are the underlying cause of caries.

49. The accumulation of these acid products causes the pH of the plaque to drop to levels sufficient to react with the hydroxyapatite of the enamel demineralizing it to soluble calcium and phosphate ions Production of acid and decreased pH is maintained until the substrate is depleted after which the plaque pH returns to its more neutral pH resting level and some recovery can take place. Dietary monosaccharides ( eg , glucose, fructose) and disaccharides ( eg , sucrose, lactose, and maltose) provide an appropriate substrate for bacterial glycolysis and acid production to cause tooth demineralization . Foods with high sugar content, particularly sucrose, which adhere to the teeth and have long oral clearance times, are more cariogenic than less retentive food stuffs such as sugar-containing liquids

50. sucrose is also used for the synthesis of extracellular polyglycans such as dextrans and levans by transferase enzymes on the bacterial cell surface . Polyglycan production contributes to aggregation and accumulation of S mutans on the tooth surface and may also serve as an extracellular storage form of substrate for other plaque bacteria.

51. Dental caries is the single greatest cause of tooth loss in the child and young adult. Its onset can occur very soon after the eruption of the teeth . The first carious lesions usually develop in pits or fissures on the chewing surfaces of the deciduous molars and result from the metabolic activity of the dental plaque that forms in these sites T he factors involved in the formation of a carious lesion are (1) a susceptible host or tooth, ( 2) the proper microflora on the tooth, and ( 3) a substrate from which the plaque bacteria can produce the organic acids that result in tooth demineralization

52. Saliva provides protection against caries, and patients with dry mouth ( xerostomia ) suffer from high caries attack rates unless suitable measures are taken. In addition to the mechanical flushing and diluting action of saliva and its buffering capacity, the salivary glands also secrete several antibacterial products. Thus , saliva is known to contain lysozyme, a thiocyanate -dependent sialoperoxidase , and immunoglobulins , principally those of the secretory IgA class

53. Cariogenic prop of strep mutans Produces lactic acid from sucrose Can live at ph as low as 4.2 • Forms large amounts of extracellular,sticky,insoluble glucan plaque matrix . • Adheres to pellicle and contributes to plaque formation.

54. Caries initially involves only the enamel and produces no symptoms . A cavity that invades the dentin causes pain , first when hot , cold, or sweet foods or beverages contact the involved tooth , and later with chewing or percussion . Pain can be intense and persistent when the pulp is severely involved

55. Control of caries involves physical removal of plaque, limitation of sucrose intake, good nutrition with adequate protein intake, and reduction of acid production in the mouth By limitation of available carbohydrates and frequent cleansing. The application of fluoride to teeth or its ingestion in water results in enhancement of acid resistance of the enamel . Control of periodontal disease requires removal of calculus ( calcifed deposit) and good mouth hygiene

56. . As it can be the source of transient bacteremia, dental plaque must be viewed as a hazard in the compromised patient The best example is the patient with heart valve damage as a result of a congenital anomaly, rheumatic fever, or a heart prosthesis. If transient bacteremia develops, the blood-borne bacteria may form vegetative growths in the heart and cause bacterial endocarditis Such patients should always be premedicated with prophylactic antibiotics before any dental procedure with the potential for causing a bacteremia is performed, including routine dental prophylaxis.

57. VIRIDANS STREPTOCOCCI The many species of the viridans streptococci are classi - fed into groups and include the Streptococcus mitis group, Streptococcus anginosus group , Streptococcus mutans group, Streptococcus salivarius group, and S bovis group Typically they are α-hemolytic, but they may also be nonhemolytic. Th e viridans streptococci are the most prevalent members of the normal microbiota of the upper respiratory tract

58. Cot… They may reach the bloodstream as a result of trauma and are a principal cause of endocarditis on abnormal heart valves. Some viridans streptococci ( eg , S mutans ) synthesize large polysaccharides such as dextrans or levans from sucrose and contribute importantly to the genesis of dental caries Rapid destruction of the valves frequently leads to fatal cardiac failure in days or weeks unless a prosthesis can be inserted during antimicrobial therapy.

59. Subacute endocarditis often involves abnormal valves (congenital deformities and rheumatic or atherosclerotic lesions ). FIGURE A: Optochin inhibition and bile solubility of S. pneumoniae . B: The growth of the viridans streptococci is not inhibited by optochin . The optochin (ethyl hydrocupreine HCl ) or P disc

60. S.N. Characteristics S. pneumoniae Viridans Streptococci 1. Morphology Lanceolate diplococci Oval or round cells in chain 2. Capsule Capsulated Non-capsulated 3. Quellung Test Positive Negative 4. Bile solubility Bile soluble Bile insoluble 5. Inulin fermentation Positive Negative 6. Optochin sensitivity Sensitive Resistant 7. Pathogenicity in mice Pathogenic Non-pathogenic 8. Hemolysis Alpha-hemolytic (under aerobic conditions) or Beta-hemolytic (under anaerobic conditions) Alpha hemolytic or non-hemolytic 9. Pathogenesis Causes pneumonia Causes mainly oral infections

61. Actinomycetes

62. These are Gram-positive rods that often occur in the form of branched filaments in young cultures. Monoinfections are rare, the most frequent case being actinomycetes -dominated endogenous polyinfections Macroscopic colonies of organisms resembling grains of sand can frequently be seen in the abscesses and sinus tracts. These colonies, called sulfur granules because they appear yellow or orange, are masses of filamentous organisms bound together by calcium phosphate

63. Laboratory Diagnosis The significance of Actinomyces isolated from contaminated specimens cannot be determined. Because the organisms are concentrated in sulfur granules and are sparse in involved tissues, a large amount of tissue or pus should be collected If sulfur granules are detected in a sinus tract or in tissue, the granule should be crushed between two glass slides, stained, and examined microscopically.

64. A. viscosus infection symptoms are indistinguishable from Actinomyces israelii or Actinomyces bovis infection symptoms. A . israelii and A. bovis infections usually cause actinomycotic infections , but sometimes and very rarely will the pathogen be A. viscosus . A . viscosus colonies test positive for catalase and negative for indole .

65. Thin, gram positive , branching rods can be seen along the periphery of the granules. Actinomyces are fastidious and grow slowly under anaerobic conditions; it can take 2 weeks or more Colonies appear white and have a domed surface that can become irregular and resembling the top of a molar

66. Actinomyces viscosus Actinomyces viscosus is a human and animal pathogen which colonises the mouths of 70% of adult humans. A. viscosus is Gram-positive, facultatively anaerobic, rod-shaped, and filamentous . It grows slowly on nonselective media, forming gray and white colonies. A. viscosus causes periodontal disease in animals and has been isolated from human dental calculus

67. Furthermore, it has been shown to cause endocarditis in humans. Therapies include treatment with penicillin, sulfadimethoxine , flucloxacillin , clindamycin, and tetracycline A. viscosus is usually resistant to vancomycin , metronidazole cefalexin , and dicloxacillin

68. Bacteroides forsythus Bacteroides have a typical gram-negative cell wall structure , which can be surrounded by a polysaccharide capsule . I t is anaerobic, fusiform bacterium , and its presence in subgingival flora has been significantly associated with severe periodontal disease However , only a few putative virulence factors have been identified in B. forsythus b ecause of the fastidious nature of its growth and the difficulties in cultivating it from the human oral cavity

69. virulence actors The virulence actors that have been identified so far are a trypsin-like protease , a sialidase , specific protease encoded by the prtH gene , and a cell surface-associated protein of B. forsythus which is involved in adhesion to fibronectin and fibrinogen

70. Porphyromonas spp Th e Porphyromonas species also are gram-negative bacilli that are part of the normal oral microbiota and occur at other anatomic sites as well. Porphyromonas species can be cultured from gingival and periapical tooth infections Porphyromonas gingivalis is a Gram-negative oral anaerobe that is involved in the pathogenesis of periodontitis ; an inflammatory disease that destroys the tissues supporting the tooth which eventually may lead to tooth loss.

71. Properties and Pathogenicity of P.gingivalis . The perturbation of epithelial cells by bacteria is the first stage in the initiation of inflammatory and immune processes which eventually cause destruction of the tissues surrounding and supporting the teeth which ultimately result in tooth loss P gingivalis can locally invade periodontal tissues and evade the host defense mechanism P gingivalis rapidly adheres to the host cell surface followed by internalization via lipid rafts and incorporation of the bacterium

72. The harsh inflammatory condition of the periodontal pocket suggests that this organism has properties that will facilitate its ability to respond and adapt to oxidative stress Virulence and Growth of Porphyromonas gingivalis : Iron utilized by this pathogen in the form of heme has been shown to play an essential role in its growth and virulence. P. gingivalis does not produce siderophores and it employs specific outer membrane receptors, proteases , and lipoproteins to acquire iron/ heme .

73. Fusobacterium spp F nucleatum is a thin rod with tapered ends (needle-shaped morphology) and is a signifcant component of the gingival microbiota as well as the genital, gastrointestinal, and upper respiratory tracts. Capnocytophaga species Capnocytophaga  spp. are long, thin gram-negative bacilli or flamentous bacilli that are slow growing, with gliding ability on agar media . They are facultatively anaerobic and require enrichment with CO2 (5-10%) for optimum growth ( capnophilic ). The organisms grow best at 35 to 37 °C on either blood or chocolate agar. 

74. which can be seen as outgrowths of colonies. They produce a substance that modifies polymorphonuclear cell chemotactic activity. Capnocytophaga ochracea , C sputigena , and Cgingivalis are members of the normal oral microbiota of humans They have been associated with severe periodontal disease in juveniles. They occasionally cause bacteremia and severe systemic disease in immunocompromised patients, especially granulocytopenic patients with oral ulcerations. Capnocytophaga canimorsus is found among the oral flora of dogs. When transmitted to humans, it occasionally causes fulminant infection in patients with asplenia or alcoholism and rarely, in healthy people. Capnocytophaga cynodegmi is associated with wound infections from dog or cat bites or scratches.

75. They do not grow on MacConkey agar. Visible colonies typically take 2 to 4 days of incubation and some strains can be pigmented in orange or pink.  Capnocytophaga  species constitute part of the normal oral microflora of humans and animals are often considered as opportunistic pathogens, that was confirmed by recent studies of microbial profiles using the human oral microbe identification microarray Clinical isolates of  Capnocytophaga   spp are classified into two broad groups: ( 1) those species found in the human oral cavity:  C. gingivalis ,  C. granulosa ,  C. haemolytica ,  C. leadbetteri , C. ochracea  and  C. sputigena  and ( 2) those species that colonize the oral cavities of dogs (and occasionally cats):  C. canimorsus   and  C. cynodegmi  

76. Actinobacillus actinomycetemcomitans Aggregatibacter actinomycetemcomitans (formerly Actinobacillus actinomycetemcomitans) is a small gram-negative coccobacillary organism that grows slowly. It causes severe periodontal disease in adolescents, endocarditis, abscesses, osteomyelitis , and other infections. It is treatable with tetracycline or chloramphenicol and sometimes with penicillin G, ampicillin, or erythromycin. The other important organism in this genus is Aggregatibacter aphrophilus (formerly Haemophilus aphrophilus and the “A” in the HACEK acronym-Haemophilus, Aggregatibacter , Cardiobacterium , Eikenella , Kingella

77. Capnocytophaga  spp. have been recovered from a variety of oral/dental sites specimens Identification and quantification of putative periodonto -pathogen Capnocytophaga  species, by commercially available rapid PCR-based methods  OR 16 rRNA . The species that colonize humans are opportunistic pathogens invading tissues as a result of interruption of the normal mucosal barriers in the healthy human oropharynx from trauma, disease or ulceration/ mucositis .

78. Esophagitis is a disease characterized by inflammation of the esophagus. The esophagus is a tube composed of a mucosal lining, and longitudinal and circular smooth muscle fibers. It connects the pharynx to the stomach; swallowed food and liquids normally pass through it.

79. Esophagitis can be asymptomatic; or can cause epigastric and/or substernal burning pain, especially when lying down or straining; and can make swallowing difficult (dysphagia). The most common cause of esophagitis is the reverse flow of acid from the stomach into the lower esophagus: gastroesophageal reflux disease (GERD) Esophagitis that happens due to a viral, fungal, parasitic or bacterial infection. More likely to happen to people who have an immunodeficiency.

80. Fungal Candida (Esophageal candidiasis) Viral Herpes simplex (Herpes esophagitis) Cytomegalovirus Porphyromonas , and Prevotella . Common causes of gastroenteritis (e.g., Salmonella and Campylobacter spp.) can be present in small numbers as asymptomatic residents; however, their detection in the clinical laboratory generally indicates disease.

81. Candida -induced esophagitis Although Candida is considered normal flora in the gastrointestinal tract of humans, it can cause disease when an imbalance exists. Generally different Candida species can create clinical syndromes, although infection with C. albicans is the most common It seems to be important to identify the type of yeast because some species are more resistant to antifungal agents than others. Local , oropharyngeal candidiasis is a common infection seen particularly in infants or older adults who wear dentures patients treated with antibiotics, chemotherapy and/or radiation therapy to the head and neck , and those with immune deficiency states, such as AIDS

82. Patients treated with inhaled steroids are also at risk. The usual symptoms of oropharyngeal candidiasis are loss of taste, and pain during eating and swallowing or when patients try to wear their dentures . The diagnosis is usually made upon the presence of white plaques in the oral cavity mucosa or under dentures, where there is usually erythema without plaques

83. Esophageal candidiasis is most common in patients with hematologic malignancies, steroid use or AIDS . Esophageal candidiasis(EC) , an AIDS-defining illness , is common among HIV infected patients. This is because approximately 10% of HIV infected patients will develop EC during their lifetime, and another 90% of all HIV infected patients will develop oropharyngeal candidiasis Interestingly, concomitant thrush is or is not present, which means that the absence of thrush does not preclude the diagnosis of esophagitis

84. A characteristic feature of Candida esophagitis is odynophagia or retrosternal pain on swallowing. The diagnosis of Candida esophagitis is usually made when white mucosal plaque-like lesions are seen on esophagogastroduodenoscopy

85. Confrmatory biopsy shows the presence of yeast and pseudohyphae with invasion of mucosal cells. An alternative diagnostic approach, particularly useful in AIDS patients, is to treat with systemic antifungal agents on the basis of the patient's history

86. Oropharyngeal candidiasis is the most common problem in HIV-infected patients. It usually coexists with significant immunosuppression – CD4 counts < 200 cells/ml . The treatment of first oropharyngeal candidiasis in this group of patients also can involve local antifungal lozenges or solutions of nystatin or clotrimazole, but in general oral fluconazole is probably a better option, especially in patients who are at risk of developing esophageal candidiasis – CD4 count < 100 cells/ml

87. The diagnosis is confirmed by performing a Gram stain or KOH preparation on the scrapings which reveals yeasts usually with pseudohyphae

88. Herpes simplex virus-induced esophagitis HSV infection of the esophagus is usually observed in patients with an impairment of immunity, but can occasionally be seen in healthy hosts That is mostly related to HSV type 1, although HSV-2 has also been reported [16]. HSV esophagitis occurs most frequently in solid organ and bone marrow transplant recipients Herpes simplex virus esophagitis usually is a consequence of reactivation of HSV with spread of virus to the esophagus through the vagus nerve or by direct extension of infection from the oral cavity into the esophagus

89. Patients usually complain about odynophagia and/or dysphagia. Fever and retrosternal chest pain can be present in about 50% of individuals. Patients also can have coexistent herpes labialis or oropharyngeal ulcers The diagnosis of herpes simplex virus esophagitis is usually based on endoscopic findings confirmed by histopathological examination. Lesions which usually form ulcers less than 2 cm involve the mucosa of the distal esophagus. These ulcers are well circumscribed and have a "volcano-like" appearance; diffuse erosive esophagitis may also be present.

90. Biopsies should be taken from the edge of an ulcer where viral cytopathic action is most likely to be seen. Histologic fndings include multinucleated giant cells, with ground-glass nuclei and eosinophilic inclusions. Immunohistochemical examination for HSV glycoproteins may also be helpful

91. The treatment of HSV esophagitis depends on the patient’s underlying immune condition . Spontaneous resolution usually occurs after 1 to 2 weeks in patients without impaired immunity, although some may respond more quickly if treated with a short course of oral acyclovir 200 mg five times a day or 400 mg three Times a day for 1 to 2 weeks. Alternatively famiciclovir 500 mg three times a day or valacyclovir 1 g three times a day can be used. Patients with severe odynophagia may require hospitalization for parenteral acyclovir therapy 5 mg/kg 3 times a day for 1 to 2 weeks

92. Those who improve quickly can be switched to oral therapy. Patients who do not respond to therapy probably are infected with a virus strain resistant to acyclovir resulting from mutations within the thymidine kinase or the DNA polymerase gene of HSV. Viruses with thymidine kinase mutations are generally cross-resistant to other drugs in this class In that case treatment with foscarnet can be an option .

93. Cytomegalovirus-induced esophagitis Cytomegalovirus (CMV) is, like HSV, a member of the Herpesviridae family. Cytomegalovirus esophagitis is observed in patients who have undergone transplantation, those undergoing long-term dialysis, HIV-infected The average time to development of CMV esophagitis after solid organ transplantation Patients undergoing bone marrow transplantation may develop CMV disease at an average of 3 months or even much earlier Studies show that even about 80% of the world's population is CMV-positive

94. Cytomegalovirus infection is a consequence of three possible mechanisms. About 60% represents primary infection which in patients with normal immunity causes few or no symptoms and CMV can persist in a latent form in most organs of the body. About 10–20% occurs in that group with a latent virus that becomes reactivated when the host's immune system becomes compromised. The last 10–20% represents superinfection

95. Cytomegalovirus esophagitis presents with fever, odynophagia , and nausea, and is occasionally accompanied by substernal burning pain. Esophagogastroduodenoscopy usually reveals large solitary ulcers or erosions seen in the distal esophagus. Ulcers seen in CMV infection tend to be linear or longitudinal and deep. A confrmatory biopsy demonstrates tissue destruction and the presence of intranuclear or intracytoplasmic inclusion bodies

96. The treatment of CMV esophagitis involves induction therapy for 3 to 6 weeks, but optimal duration of therapy is not clear. Maintenance treatment is controversial. In general, intravenous ganciclovir 5 mg/kg or foscarnet 90 mg/kg is recommended for induction therapy. Maintenance therapy with oral valganciclovir 900 mg twice a day seems to be an option in patients who have had a relapse . Reduction therapy is required again before maintenance treatment