Gram positive and negative bacteria pptx

Gram negative andvpositive bacteria

1. Heba Gomaa Abd Elraheem Assistant Professor of pediatrics Pediatric Hematology, Oncology and BMT Ain Shams University Gram positive and negative infection

2. Disclosure I have NO any disclosure or conflicts of interest with the presented material in this presentation

3. Introduction, what is the bacteria?. Classification of bacteria. Gram stain Gram positive and negative bacteria Difference Classifications Clinical manifestations How to diagnose. Treatment.

4. Bacteria : Bacteria consist of only a single cell. There are thousands of species of bacteria, but all of them are basically one of three different shapes.

5. Difference between human cell and bacterial cell

6. Difference between human cell and bacterial cell

7. Classification of bacteria:

8. Classification of bacteria:

9. Classification of bacteria:

10. Classification of bacteria:

11. Classification of bacteria:

12. Classification of bacteria:

13. Classification of bacteria:

14. Classification of bacteria:

15. Classification of bacteria:

16. Classification of bacteria:

17. Classification of bacteria:

18. Gram Stain :

19. Gram stain

20. Gram stain :

21. Gram stain

22. Bacterial cell wall :

23. Bacterial cell wall :

24. Bacterial cell wall :

25. Bacterial cell wall :

26. Difference between Gram-positive and negative bacteria

27. Difference between Gram-positive and negative bacteria

28. Gram stain

29. Gram stain

30. Gram- Positive Bacteria :

31. Classification of Gram-Positive Bacteria

32. Classification of Gram-Positive Bacteria

33. Gram- Positive Cocci

34. Gram- Positive Cocci :

35. Staphylococcus spp.

36. Type of infections:

37. Type of infections:

38. Staphylococcus aureus Type of infections

39. Staphylococcus aureus Type of infections

40. Staphylococcus aureus Type of infections

41. Staphylococcus aureus

42. Staphylococcus aureus

43. Staphylococcus aureus

44. Staphylococcus aureus

45. Staphylococcus aureus

46. Other Staphylococci

47. Streptcoccus spp :

48. Streptococcal types :

49. Gram- Positive Cocci :

50. Streptococcal infection :

51. Streptococcal infection

52. I-Alpha-hemolytic Streptococcus

53. Streptococcus Pneumoniae ( Pneumococcus ): Epidemiology Most common cause of community acquired pneumonia Classic Symptoms Shaking rigors Fever Purulent sputum Pleuritic chest pain Dyspnea

54. Streptococcus Pneumoniae ( Pneumococcus ):

55. Streptococcus Pneumoniae ( Pneumococcus ):

56. Streptococcus Pneumoniae ( Pneumococcus ):

57. Streptococcus Pneumoniae ( Pneumococcus ) : Lab CBC WBC elevated with left shift Gram stain Gram positive encapsulated organisms Elongated lancet shaped diplococci Blood Culture Positive in only 33% of cases Sputum culture Positive in only 40% of pneumococcal pneumonias Radiology Chest X-ray Lobar consolidation (often lower lobe) patchy infiltrates

58. Streptococcus Pneumoniae ( Pneumococcus ) management : Penicillin Sensitive Ampicilin IV or Amoxicillin PO Erythomycin Azithromycin Clarithromycin Penicillin G IV Doxycycline Oral second generation cephalosporin Parenteral third generation cephalosporin

59. Streptococcus Pneumoniae ( Pneumococcus ) management: High-Level Penicillin Resistance Broad spectrum Fluoroquinolone Levofloxacin Gatifloxacin Grepafloxacin Moxifloxacin Sparfloxacin Parenteral third generation Cephalosporin High dose Ampicillin Vancomycin IV with or without Rifampin

60. Streptococcus Pneumoniae ( Pneumococcus ) management:

61. II-Beta-hemolytic Streptococcus

62. Streptococcus Pyogenes Infections

63. Streptococcus Pyogenes Infections

64. Streptococcus Pyogenes Infections

65. Streptococcus Pyogenes Infections

66. Streptococcus Pyogenes Infections

67. Streptococcus agalactiae

68. Streptococcus agalactiae Pathophysiology Group B Beta-hemolytic streptococcus infection Perinatal transmission Delivery via a birth canal colonized with GBS Incidence of U.S. vaginal GBS colonization: 15-20% Onset of infection (Mean onset 20 hours of life) Early onset neonatal disease (<6 days of life in 80%) Sepsis Pneumonia Late onset neonatal disease of sepsis or mengitis

69. Streptococcus agalactiae Labs: Maternal Screening GBS Culture Management -Sepsis (treat for 10-14 days) Pencillin G 200,000 units/kg/day divided q4-6 hours -Meningitis (treat for 14-21 days) Penicillin G 400,000 units/kg/day divided q2-4 hours Prevention Perinatal Group B Streptococcus Prophylaxis Prognosis Mortality 10-40%

70. Enterococcus I-Characteristics Gram Positive Cocci Previously defined as Group D Streptococcus II-Organisms Enterococcus faecalis Enterococcus faecium III-Important clinical infections caused by  Enterococcus  include  urinary tract infections ,  bacteremia ,  bacterial endocarditis ,  diverticulitis , and  meningitis . Sensitive strains of these bacteria can be treated with  ampicillin ,  penicillin  and  vancomycin .  Urinary tract infections can be treated specifically with  nitrofurantoin , even in cases of vancomycin resistance

71. Gram-Positive Rod

72. Classification of Gram-Positive Bacilli

73. Classification of Gram-Positive Bacteria

74. CLOSTRIDIUM SPECIES All are gram positive, anaerobic, spore forming rods that are motile . They are in soil, water& human GIT. Four clostridial species are important human pathogens : C. botulinum , C. difficile , C. perfringens , C. tetani .

75. Clostridium tetani PROPERTIES and EPIDEMIOLOGY: Motile Gram- Positive Rod Anaerobic move with the help of a flagella Spore forming, Spores are well spread in the soil & feces of horses & other animals. Entry occurs through a wound in generalized &localized tetanus. Addicts receive this through skin popping, Neonates receive it through the contaminated umbilicus or circumcision wound. CNS disease develops through most commonly an ear infection (rare).

76. Clostridium tetani Pathogenesis : -The organism is not invasive & the germination of spores is assisted by necrotic tissues, calcium salts & associated pyogenic infections and form vegetative cells. -The disease is mediated by an exotoxin single serologic type of toxin tetanospasmin ; produced by vegetative cells.

77. Clostridium tetani (Diseases and clinical manifestation) Generalized disease (incubation 4 days to weeks) Involvement of muscles Bulbar muscles; lockjaw, Risus Sordonicus , difficulty in swallowing, Involvement of skeletal muscles; Opisthotonos . The patient is fully conscious & pain is severe. Death is due to respiratory failure. Involvement of autonomic nervous system Sweating Hyperthermia Cardiac arrhythmias Fluctuation in blood pressure

78. Clostridium tetani Localized disease Spasm in the muscles of the area of initial injury. May proceed to generalized disease. Neonatal disease; Generalized disease in the neonates. A septic umbilical stump is usually seen & mother will not be having immunization. CNS disease ; There is isolated or combined involvement of cranial nerves but the 7 th nerve is most commonly involved. An infection can commonly be found in ear or there is a history of such infection. The prognosis is extremely poor.

79. Clostridium tetani Diagnosis: Clinically. There is history of injury in 50% of cases. Microscopy can reveal both forms vegetative & spores. Typical tennis racket or drum stick appearance is suggestive of the C tetani

80. Clostridium botulinum PROPERTIES and EPIDEMIOLOGY: Gram positive spore forming rod. Spores are heat resistant. Motile with flagella It is worldwide in distribution. Found in soil & animals feces. Disease is caused by ingestion of smoked canned meat predominantly. Honey may be responsible for infantile botulism.

81. Clostridium botulinum Pathogenesis : -The anaerobic conditions in such foods cause germination of spores & the vegetative bacteria produce toxins (7 types A-G). -An exotoxin (E) inhibits the release of Ach at the neuromuscular junction. The toxin is destroyed by boiling for 20 minutes. -There is flaccid paralysis is contrast to tetanus where there is spastic paralysis. -Death results from respiratory failure.

82. Clostridium botulinum (Diseases and clinical manifestation) Classic food borne botulism 18 to 24 hours incubation is followed by. Early Symptoms; GIT symptoms are although not regularly present but if occur are the first symptoms, include nausea vomiting constipation. Followed by dizziness, lassitude & weakness. Late symptoms; Diplopia . Flaccid paralysis Dysphagia . Difficulty speaking Respiratory failure & death. Untreated cases are sure death. Infantile botulism Occurs In the first month of life. Develop poor feeding & weekness . Followed by flaccidity “floppy baby syndrome” It is one cause of SIDS. Honey has been implicated as a cause of the disease. Infants recover with supportive therapy in most cases.

83. Clostridium botulinum diagnosis: Toxin is found in the Serum Remaining food. Antigenic type of toxin is elaborated by using specific antitoxin in mice. The organism may be isolated from the remaining food. The organism can be detected in feces.

84. Clostridium Difficile PROPERTIES and EPIDEMIOLOGY: Gram positive spore forming rod, strict anaerobe. Spores are commonly found in the hospital environment. Some healthy individuals reside them in the colon Antibiotic therapy increases the growth & overgrowth can result in disease. Spores are commonly found in the hospital washrooms, beds, & is a serious source of nosocomial infections. Commonly involve antibiotics are ampicillin amoxacillin , clindamycin & the third generation cephalosporins . Risk factors for C. difficile –associated colitis include advanced age & hospitalization

85. Clostridium Difficile PROPERTIES and EPIDEMIOLOGY: Toxins and Enzymes: Produce toxin A an enterotoxin binds to the brush border & is cytotoxic . It causes hemorrhagic necrosis. Toxin B destroys actin & hence disrupts the cytoskeleton. Both are exotoxins . Enzymes Hyaloronidase

86. Clostridium Difficile Pseudomembranous colitis - Disruption of the normal colonic flora by antibiotics allows C. difficile overgrowth. The organism in the brush border produce toxins that disrupt the mucosal barrier. Inward spread of the organism produce an i nflammatory response so intense that the exudate & necrotic debris sprout out into the lumen. This debris form a carpet over the lumen giving the appearance of a membrane called pseudomembrane

87. Clostridium Difficile diagnosis: There is watery or bloody diarrhea following an antibiotic administration. Associated with abdominal cramps fever, leukocytosis . On endoscopy a reddish brown colored membrane with microabcesses is seen. Diagnosis is made by isolating the organism & demonstrating the toxins.

88. Clostridium Perfringens PROPERTIES : Large, boxcar-shaped, aerotolerant , rapidly growing rods. Subtypes A to E defined based on production of major toxins. Clostridium grows well at body temperature; In stressful environments, the bacteria produce spores that tolerate extreme conditions.

89. Clostridium Perfringens Spores are characterized on the basis of position, size and shape Most Clostridium spp., including C. perfringens and C. botulinum , have ovoid subterminal (OST) spores C. tetani have round terminal (RT) spores

90. Clostridium Perfringens Pathogenesis: The spores that are present in soil can contaminate food. Spores are very heat resistant so are not activated by usual cooking. They especially grow in reheated meat products to a very large number. Food poisoning occurs usually due to consumption of reheated meat. Although there are thirteen known toxins & enzymes following are inportant . Alpha toxin; lecithinase splits cell membrane lecithin. Theta toxin has hemolytic & necrotizing effects Enterotoxin

91. Clostridium Perfringens Pathogenesis: Spores germinate at low oxygen in traumatized tissue. Produce gas the distension of the tissue interferes with the blood supply. Secretion of hyaluronidase favors spread. Tissue necrosis extends leading to increased growth hemolytic anemia, toxemia & death. Mixed infection is the rule. Bacteremia frequenly occurs in cancer patient .

92. Clostridium Perfringens diseases: Gas gangrene . Food poisoning (type A) Necrotizing enterocolitis (type C) Cellulitis and fasciitis

93. Clostridium Perfringens diagnosis: Diagnosis is easily made clinically in case of gangrene. Smears show typical organism Spores are not seen Cultured anaerobically Double zone of hemolysis Lecithinase is seen in the Negler reaction Acidifies litmus milk.

94. BACILLUS SPECIES Bacillus anthracis Bacillus cereus

95. Bacillus anthracis Large, gram-positive, aerobic, spore-forming rods that produce exotoxins . Central spores that develop under all conditions except in the living body. Nonmotile (unlike other bacilli)

96. Bacillus anthracis Humans get the infection usually from an animal contact. Spores can also be inhaled not from person to person. Contaminated meat ingestion leads to GIT anthrax. Based on the production of two exotoxins collectively called anthrax toxin. Edema factor Lethal factor.

97. Bacillus anthracis diagnosis: Smears with no motility gram positive rod in chains. Culture show non hemolytic colonies. PCR is used in special labs in cases of terrorism. Direct fluorescence ELISA can also be used for detection.

98. Bacillus anthracis clinical manifestations: Cutaneous Anthrax 95% human cases are cutaneous infections 1 to 5 days after contact Small, pruritic , non-painful papule at inoculation site Papule develops into hemorrhagic vesicle & ruptures Slow-healing painless ulcer covered with black eschar surrounded by edema Infection may spread to lymphatics w/ local adenopathy Septicemia may develop 20% mortality in untreated cutaneous anthrax Gastrointestinal (Ingestion) Anthrax 100% fatal Abdominal pain, nausea , vomiting and bloody diarrhea Hemorrhagic ascites Paracentesis fluid may reveal gram-positive rods Inhalation Anthrax 100% fatal (pneumonic) woolsters disease Meningitis may complicate cutaneous and inhalation forms of disease Pharyngeal anthrax Fever Pharyngitis Neck swelling

99. Bacillus anthracis clinical manifestations: Cutaneous Anthrax The typical lesion of cutaneous anthrax is a painless ulcer called black eschar . It is black with local edema. It is called malignant pustule

100. Bacillus cereus Microscopically very similar two bacillus anthracis but are motile may be gram variable. Cause hemolysis on blood agar in contrast to B anthracis .

101. Bacillus cereus The spores germinate when kept for some hours. Reheated fried rice. Portal is GIT . Produce two enterotoxxins.One of them acts similar to cholera toxin this leads to increase in cAMP in the enterocytes leading to diarrhea. Other toxin is a superantigen To type of food poisoning occur. One with vomiting incubation 4 hours. One with watery diarrhea incubation 18 hours.

102. Corynebacterium PROPERTIES Corynebacterium diphtheria is the organism that causes diphtheria Gram positive aerobic rods. Individual organism appears club shaped. They are arranged in palisade in either V or L forms.

103. Corynebacterium Epidemiology : -Humans are natural host -Both toxigenic & nontoxigenic strains reside in the human upper respiratory tract. -The disease is transmitted by airborne droplets. -The organism can infect the preexisting wounds or lesions seen commonly in the tropical countries.

104. Corynebacterium Pathogenesis: - It causes disease by both invasion & toxin production. -The organism first adheres to the throat. -It then produces exotoxin . The host response. A local inflammatory reaction takes place. The exudate is fibrinous . This exudate forms a grey colored pseudomembrane on the surface of the throat. This membrane is thich hard & adheres firmly two the underlying tissue. When removed the surface bleeds. Antibody against this toxin is protective

105. Corynebacterium Clinical features -The disease is still a problem in the developing countries. -Rarely seen before the age of 1 because of maternal antibodies. - Peak : 1-5 years, 5-10 years- decreases thereafter. -There is fever, chills, hoarseness of voice, sore throat, nasal discharge, malaise, lethargy & lymphadenopathy . -Within two to three days, a thick coating can build up in the throat. -This makes it difficult to breath & swallow. -On clinical examination there is a thick membrane over the throat that if pulled leads to bleeding. The toxin may be absorbed into the blood stream and may cause damage to the heart, kidneys and nerves.

106. Corynebacterium Clinical features: Diphtheria causes a characteristic swollen neck, sometimes referred to as “bull neck”

107. Corynebacterium Clinical features: A second type of diphtheria can affect the skin, causing the typical pain, redness and swelling associated with other bacterial skin infections. Ulcers covered by a gray membrane also may develop in cutaneous diphtheria. Most commonly seen in the developing countries & poor hygienic states

108. Corynebacterium Complications: -Extension of the membrane into the airways can lead to asphyxia & cyanosis. - Myocarditis can result leading to arrhythmia & collapse. -Nerve weakness & paralysis especially of the cranial nerves. -Peripheral neuritis of the extremities can also result.

109. Corynebacterium Diagnosis and treatment: -Labs CBC Leukocytosis Throat culture (+ for corynebacterium org.) -Management Diphtheria antitoxin Erythromycin 20-25 mg/kg q12 hours IV for 7-14 days -Prevention DTP/ DTaP vaccination

110. Listeria monocytogenes

111. Listeria monocytogenes

112. Listeria monocytogenes

113. Listeria monocytogenes diagnosis and treatment:

114. Actinobacteria Is a large group of Gram-positive bacteria. Two bacteria are of medical importance in this phylum belong to family Actinomycetes Actinomyces israelii Nocardia astroiditis . Mycobacteria also belong to this but will be discussed separately as they are not gram positive & have very different characteristics

115. Actinobacteria

116. Myobacterium

117. Myobacterium tuberculosis:

118. Myobacterium tuberculosis :

119. Myobacterium tuberculosis:

120. Thank you Thank You

121. Gram-Negative bacteria :

122. Gram-Negative bacteria Cocci : Neisseria . Moraxella catarrhalis . Bordetella pertussis

123. Neisseriaceae : Neisseria meningitidis Neisseria gonorroeae

124. Neisseria gonorrhoeae :

125. Neisseria gonorrhoeae :

126. Neisseria gonorrhoeae :

127. Neisseria gonorrhoeae

128. Neisseria gonorrhoeae

129. Neisseria gonorrhoeae Gonorrhoeae in newborn Infected as they pass through birth canal. Cause eye inflammation and blindness. Prevented by prophylaxis at birth. ( silver nitrate, antibiotics) Older children (>1 year): considered possible evidence of sexual abuse

130. Neisseria gonorrhoeae Gonorrhoeae in men and women Conjunctivitis usually autoinoculation in adults. Symptom: eye irritation with purulent conjunctival exudate Disseminated gonococcal infection (DGI) occurs infrequently. More common in women than in men associated with gonococcal strain that produce bacteremia without associated urogenital symptoms clinical manifestations : skin lesions, arthralgias , arthritis, hepatitis, myocarditis , endocarditis , meningitis

131. Neisseria gonorrhoeae :

132. Neisseria meningitidis :

133. Neisseria meningitidis :

134. Neisseria meningitidis :

135. Neisseria meningitidis :

136. Moraxella catarrhalis - Aerobic Gram-Negative cocci - Represents less than 5% of all pneumonias - More common in COPD - Lobar consolidation is rare, Sinusitis and ear infection Labs Gram stain Kidney bean shaped gram negative diplococci Radiology Chest xray patchy bronchopulmonary infiltrate

137. Bordetella pertussis Small, aerobic, nonmotile coccobacillus B. pertussis is the most important Causes pertussis , also called whopping cough Most cases of disease are in children Produce various adhesins and toxins, including pertussis toxin, that mediate the disease Bacteria are first inhaled in aerosols and multiply in epithelial cells Incubation period 1-2 weeks Then progress through three stages of disease( Catarrhal, Paroxymal and Convalescence)

138. Bordetella pertussis Diagnosis Symptoms of pertussis are usually diagnostic Treatment Primarily supportive Antibacterial drugs have little effect on the course of the disease Prevention Immunization with the DPT vaccine

139. Gram-Negative bacteria :

140. Enteric infections Overview of symptoms non-inflammatory nausea vomiting diarrhea inflammatory Dysentery (severe diarrhea containing mucus and/or blood) Invasive (systemic) Typhoid Fever (enteric fever)

141. Common” organisms associated with enteric infections :

142. Pathogenesis of enteric bacteria Host factors personal hygiene fecal-oral contamination gastric acidity enteric microflora specific immunity

143. Pathogenesis of enteric bacteria Microbial factors Toxins Neurotoxins usually ingested as preformed toxins Staphylococcal toxins ( Staph. aureus ) Botulinum toxin ( Clostridium. botulinum ) Enterotoxins having a direct effect on intestinal mucosa (elicit fluid secretions) Cholera toxin ( Vibrio . cholerae ) E. coli toxins Cytotoxins mucosal destruction (often see dysentery) Shigella dysenteriae Clostridium perfringens S. aureus Clostridium difficile

144. Treatment : Fluid/electrolyte replacement fluid alone for mild cases dehydration most common cause of death due to diarrheal disease Antibiotics not used unless systemic/severe e.g. enteric fever immunosuppressed Antibiotic prophylaxis for those traveling to high-risk countries (esp. immunocompromised )

145. Enterobacteriaceae Gram negative rods most are motile ( peritrichous flagella) most are encapsulated LPS is a virulence factor many have “ serum resistance ” inhibitions of complement proteins ( Ab’s can’t attack) Associated with: Enteric (GI) infections Bacteremia (bacteria in the blood) UTIs (urinary tract infections)

146. Enterobacteriaceae members of family commonly associated with human disease: Escherichia Salmonella Shigella Yersinia Klebsiella Serratia Proteus

147. Enterobacteriaceae

148. Enterobacteriaceae diseases :

149. E. coli

150. E. coli

151. E. coli

152. E. coli

153. E. coli

154. E. coli

155. Salmonella

156. Salmonella

157. Salmonella

158. Salmonella

159. Salmonella

160. Salmonella

161. Salmonella

162. Salmonella

163. Salmonella

164. Shigella

165. Shigella

166. Shigella

167. Shigella

168. Proteus

169. Proteus

170. Proteus

171. Klebsiella pneumoniae

172. Klebsiella pneumoniae

173. Klebsiella pneumoniae

174. Klebsiella pneumoniae

175. Others

176. Vibrio cholerae

177. Vibrio cholerae

178. Vibrio cholerae

179. Vibrio cholerae

180. Helicobacter pylori

181. Helicobacter pylori

182. Helicobacter pylori

183. Helicobacter pylori

184. Helicobacter pylori

185. Helicobacter pylori

186. Campylobacter

187. Campylobacter

188. Yersinia Enteric pathogens : Y. enterocolitica , Y. pseudotuberculosis Y. pestis – plague (fleas and rats) Gram negative, pleomorphic rods primarily found in animals (rodents, swine, cattle, etc) – all are zoonotic diseases

189. Yersinia Bubonic and Pneumonic plague formation of bubos bacteria resists phagocytosis painful inflammatory lesions Pneumonic plague – high mortality (90% of untreated) highly infections

190. Yersinia Y. enterocolitica more common than other enteric Yersinia sp. acute enterocolitis mesenteric lymphadenitis (can mimic appendicitis) over 60 different serotypes serotypes 3, 8 and 9 account for most human infections ingestion of contaminated food/milk (can grow at lower temperatures , 4 ° C) associated with a blood transfusion septicemia

191. Yersinia

192. Yersinia Diagnosis for Yersinia isolation of organism from stool or blood sample may need to do “cold enrichment” growth at 4-7 ° C for 28 days with weekly subculture on SS agar Therapy Plague antibiotics (control rodent population) Enteric infections: often self-limiting (except if progress to septicemia)

193. Pseudomonadaceae Characteristics Aerobic Gram Negative Rod Family: Pseudomonadaceae Pseudomonas aeruginosa Pseudomonas mallei ( Glanders )

194. Pseudomonas aeruginosa

195. Pseudomonas aeruginosa

196. Pseudomonas aeruginosa

197. Pseudomonas aeruginosa

198. Legionellaceae Family: Legionellaceae Legionella pneumophila

199. Legionellaceae Pathophysiology Aerobic, intracellular, Gram negative rod Virulent organism More severe disease than other atypical pneumonia Transmission Optimal conditions for growth Temperature: 89 to 113 F water Stagnant water Transmission Waterborne Freshwater or moist soil near ponds Air conditioning Condensers Cooling towers Respiratory therapy equipment Showers or water faucets Whirlpools Incubation Two to ten days

200. Legionellaceae Symptoms Prodrome for 12-48 hours Malaise Myalgia HA Symptoms for 2-3 days Fever to 40.5 C persists for 8-10 days GI symptoms- 20-40% of cases Nausea/vomiting Diarrhea Later Symptoms: Cough Minimal to no sputum production Slightly blood tinged sputum Signs Severe respiratory distress Confusion Disorientation

201. Legionella pneumophila Complications Respiratory failure (20-40% of cases) Extrapulmonary complications Myocarditis / pericarditis Prosthetic valve endocarditis Glmoerulonephritis Pancreatitis Peritonitis

202. Radiology: chest x-ray Small pleural effusions Unilateral parenchymal infiltrates Round, fluffy opacities Spread contiguously to other lobes Progresses to dense consolidation Progresses to bilateral infiltrates Legionella pneumophila

203. Legionella pneumophila Labs CBC leukocytosis leukopenia Erythrocyte Sedimentation Rate Elevated markedly LFTs increased Sputum Exam Fluorescent antibody studies of sputum Legionella can not be seen on gram stain

204. Legionella pneumophila Diagnosis Legionella urine antigen testing High sensitivity/ serogroup 1 Serogroup 1 (LP1) causes most U.S. cases Sputum Culture - to ID other serogroups Urine antigen and sputum culture all cases Legionella Serologies Legionella fourfold titer rise to >= 1:128 or Legionella titer >= 1:256

205. Legionella pneumophila Management (Antibiotic course for 21 days) Azithromycin IV Levofloxacin IV Trovafloxacin IV Erythromycin IV Add Rifampin in immunocompromised or severe disease Course Response to antibiotics may not be seen for 4-5 days Up to 15% mortality in some studies

206. Haemophilus influenzae Most strains have a polysaccharide capsule that resists phagocytosis and is used in classification of the bacteria H.influenzae type b is the most significant Was the most common form of meningitis in infants prior to the use of an effective vaccine Can cause a number of other diseases in young children Use of the Hib vaccine has eliminated much of the disease caused by H.influenzae b Other strains still cause a variety of diseases

207. Haemophilus influenzae

208. Miscellanous Bacterial Pathogens Stain pink in a Gram stain but differ from typical Gram-negative organisms Have different morphology, growth habits, or reproductive strategies Traditionally discussed separately due to their unique features

209. Spirochetes Thin, tightly coiled, helically shaped bacteria Moves in a corkscrew fashion through its environment This movement is thought to enable pathogenic spirochetes to burrow through their hosts’ tissues 3 genera cause human disease Treponema , Borrelia , and Leptospira

210. Treponema pallidum Cannot survive in the environment Lives naturally only in humans as an obligate parasite Causative agent of syphilis Syphilis occurs worldwide Transmission is almost solely via sexual contact Endemic among sex workers, men who have sex with men, and users of illegal drugs Can also be spread from an infected mother to her fetus Often results in the death of the fetus or in mental retardation and malformation

211. Treponema pallidum pallidum Syphilis can proceed through four stages Primary- symptoms associated with the initial infection Secondary- related to spread of the organisms away from the site of the original infection Latent Tertiary syphilis

212. Primary Syphilis Symptoms include: Chancre that should heal by itself in 3-6 weeks painless genitals Mouth Skin rectum Enlarged lymph nodes near the chancre the chancre 217

213. Secondary Syphilis Spotted rash all over Fever general ill feeling loss of appetite muscle aches joint pain enlarged lymph nodes hair loss may occur. 218

214. Tertiary Syphilis Cardiovascular syphilis causes aneurysms or valve disease Central nervous system disorders (neurosyphilis) Infiltrative tumors of skin, bones, or liver (gumma) 219

215. Diagnosis, Treatment, and Prevention Diagnosis Primary, secondary, and congenital can be readily diagnosed with antibody tests against bacterial antigens Tertiary syphilis is difficult to diagnose Treatment Penicillin is the drug of choice except with tertiary syphilis which is a hyperimmune response and not an active infection Prevention Abstinence and safe sex are the primary ways to avoid contracting syphilis

216. Borrelia Lightly staining, Gram-negative spirochetes Cause two diseases in humans Lyme disease Relapsing fever

217. Lyme Disease Borrelia burgdorferi is the causative agent Bacteria are transmitted to humans via a tick bite Hard ticks of the genus Ixodes are the vectors of Lyme disease

218. 223

219. Lyme Disease Pathology Shows a broad range of signs and symptoms 3 phases of disease in untreated patients In most cases an expanding red “bull’s eye” rash occurs at the site of infection Neurological symptoms and cardiac dysfunction Severe arthritis that can last for years Pathology of this stage is largely a result of the body’s immune response

220. Lyme Disease Pathology The increase of cases is a result of humans coming in closer association with ticks infected with Borrelia Antimicrobial drugs can effectively treat the first stage of Lyme disease Treatment of later stages is difficult because symptoms result from the immune response rather than the presence of bacteria Prevention is best achieved by taking precautions to avoid ticks

221. Relapsing Fever 2 types of relapsing fever Epidemic relapsing fever Endemic relapsing fever

222. Epidemic Relapsing Fever Mortality rate is 1% with treatment; 30-70% without treatment Transmitted by lice Mortality rate is 1% with treatment; 30-70% without treatment

223. Endemic Relapsing Fever Several Borrelia species can cause this disease Transmitted to humans by soft ticks of the genus Ornithodoros

224. Relapsing Fever Both types of relapsing fever are characterized by recurring episodes of fever and septicemia separated by symptom free intervals Pattern results from the body’s repeated efforts to remove the spirochetes,which continually change their antigenic surface components

225. Relapsing Fever 230 Observation of the spirochetes is the primary method of diagnosis Successful treatment is with antimicrobial drugs Prevention involves avoidance of ticks and lice, good personal hygiene, and use of repellent chemicals

226. Mycoplasmas Smallest free-living microbes Lack cytochromes, enzymes of the Krebs cycle, and cell walls Often have sterols in their cytoplasmic membranes which other prokaryotes lack Require various growth factors that must be acquired from a host or supplied in laboratory media Can colonize the mucous membranes of the respiratory and urinary tracts

227. Mycoplasma pneumoniae Attaches specifically to receptors located at the bases of cilia on epithelial cells lining the respiratory tracts of humans Causes primary atypical pneumonia, or walking pneumonia Symptoms such as fever, headache, and sore throat are not typical of other types of pneumonia Not usually severe enough to require hospitalization or to cause death Spread by nasal secretions among people in close contact

228. Mycoplasma pneumoniae Diagnosis is difficult because mycoplasmas are small and grow slowly Prevention can be difficult because patients can be infective for long periods of time without signs or symptoms

229. Rickettsias Extremely small (not much bigger than a smallpox virus) Appear almost wall-less due to the small amount of peptidoglycan present Obligate intracellular parasites Unusual because they have functional genes for protein synthesis, ATP production, and reproduction Three genera cause disease in humans Rickettsia , Orienta , and Ehrlichia

230. Table 21.1 Characteristics of Rickettsias

231. Rocky Mountain Spotted Fever 236 Symptoms usually develop about 2 to 14 days after the tick bite. They may include: Chills & Fever Severe headache Muscle pain Mental confusion & Hallucinations Rash Abnormal sensitivity to light Diarrhea Excessive thirst Loss of appetite Nausea &Vomiting Spread by ticks

232. Endemic Typhus 237 Chills Cough Delirium High fever (104 degrees Fahrenheit) Joint pain ( arthralgia ) Light may hurt the eyes Low blood pressure Rash that begins on the chest and spreads to the rest of the body (except the palms of the hands and soles of the feet) Severe headache Severe muscle pain Stupor Spread by fleas

233. Epidemic Typhus 238 Abdominal pain Spread by lice Backache Dull red rash that begins on the middle of the body and spreads Extremely high fever (105 - 106 degrees Fahrenheit), which may last up to 2 weeks Hacking, dry cough Headache Joint pain (arthralgia) Nausea Vomiting

234. Chlamydias Do not have cell walls Have two membranes but without any peptidoglycan between them Grow and multiply only within the vesicles of host cells Have a unique developmental cycle involving two forms Both forms can occur within the phagosome of a host cell

235. Chlamydia trachomatis Has a limited host range One strain infects mice, all others infect humans Infect the conjunctiva, lungs, urinary tract, or genital tract Enters the body through abrasions and lacerations Clinical manifestations result from the destruction of infected cells at the infection site, and from the resulting inflammatory response

236. Chlamydia trachomatis Causes two main types of disease Sexually transmitted diseases Causes the most common sexually transmitted disease in the United States Ocular disease called trachoma Occur particularly in children Endemic in crowded, poor communities with poor hygiene, inadequate sanitation, and inferior medical care

237. Chlamydia—Rates by Sex, United States, 1990–2009 NOTE: As of January 2000, all 50 states and the District of Columbia had regulations that required chlamydia cases to be reported. 2008 2006 2004 2002 2000 1998 1996 1994 1992 1990 Total Women Men 100 200 300 400 500 600 Rate (per 100,000 population) Year

238. Sexually Transmitted Diseases Lymphogranuloma veneruem Characterized by a transient genital lesion and swollen, painfully inflamed, inguinal lymph nodes Occurs in three stages Initial stage Produces a lesion at the infection site that is small painless, and heals rapidly Second stage Buboes develop at the infection site

239. Sexually Transmitted Diseases Third stage Only some cases progress to this stage Characterized by genital sores, constriction of the urethra, and genital elephantiasis Most infections in women are symptomatic but men may or may not have symptoms Women can develop pelvic inflammatory disease if reinfected with C. trachomatis

240. Trachoma Disease of the eye Leading cause of nontraumatic blindness in humans Bacteria multiply in the conjunctival cells resulting in scarring The scarring causes the eyelashes to turn inwards and abrade the eye that can eventually result in blindness

241. Trachoma Typically a disease of children who have been infected during birth Infection of the eye with bacteria from the genitalia can also result in disease

242. Diagnosis, Treatment, and Prevention Diagnosis Demonstration of the bacteria inside cells from the site of infection Treatment Antibiotics can be administered for genital and ocular infections Surgical correction of eyelid deformities from Trachoma may prevent blindness

243. Diagnosis, Treatment, and Prevention Prevention Abstinence and safe sex can prevent sexually transmitted chlamydial infection Blindness can only be prevented by prompt treatment with antibacterial agents and preventing reinfections

244. Bartonella Gram-negative aerobic bacilli Found in animals but only cause disease in humans 3 species are pathogenic Bartonella bacilliformis Bartonella quintana Bartonella henselae

245. Bartonella bacilliformis Bartonellosis - Carrión’s Disease Transmitted by blooding-sucking sand flies 250 Acute phase: ( Carrion's disease ) fever pallor, malaise, nonpainful hepatomegaly, jaundice, lymphadenopathy, splenomegaly. This phase is characterized by severe hemolytic anemia and transient immunosuppression. The case fatality ratios of untreated patients exceeded 40% but reach around 90% when opportunistic infection with Salmonella occurs.

246. Bartonella quintana Trench fever Spread person to person by human body lice Also causes disease in immunocompromised patients The disease is classically a five-day fever of the relapsing type

247. Bartonella henselae Cat scratch fever Introduced into humans through cat scratches or bites

248. Antibiotics

249. Mechanism of action of antibiotics:

250. Resistance and Cross resistance:

251. Questions ??????