Bacteriology Edited 1

2017
2017
Part one:
[BACTERIOLOGY]
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Bacteriology 2017
Content Page number
Staphylococcus 3
Streptococcus 4
Neisseria 11
Corynebacterium 15
Bacillus 16
Clostridium 17
E.coli 23
Klebsiella 25
Proteus 25
Pseudomonas 26
Salmonella 27
Shigella 29
Brucella 30
Vibrio 32
Treponema 37
Pertussis 38
Chlamydia 39
Mycobacterium 42
Antibiotic notes 49
Sepsis and septic shock 57
Surgery notes 60
Food poisoning 65
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GRAM POSETIVE COCCI

 Genus : staphylococcus
o Micro
Genus features :
-Gram-positive cocci in clusters
-Catalase positive (streptococci are catalase negative)
Species of Medical Importance ( s.aureus , s.epidermis(albus) , s.saprophyticus ).
1. Staphylococcus aureus
o Distinguishing Features
-Small, yellow colonies on blood agar→ staphyloxanthin enzyme
-β-hemolytic
-Coagulase positive (all other Staphylococcus species are negative)
-Ferments mannitol on mannitol salt agar
o Pathogenesis
-Protein A binds Fc component of IgG→ inhibits phagocytosis.
-Coagulase: converts fibrinogen to fibrin clot
-Exotoxins:
1.Enterotoxins: fast acting, heat stable→ food poisoning
2.Toxic shock syndrome toxin-1 (TSST-1): superantigen→ binds MHC II with CD4 non
specifically causing polyclonal T cell activation.
3.Exfolatins: skin-exfoliating toxins (involved in scalded skin syndrome [SSS])
and bullous impetigo.
o Medicine
 Diseases:
1-Cutaneous infections in the form of :
A-Folliculitis → superficial hair follicle inflammation.
B-Furuncle (boil) → folliculitis progressing into abscess .
C-Carbuncle→ interconnection of abscesses .
D-Impetigo →bulluos form of impetigo mostly in the newborns.
2-osteomyelitis →most common cause
3- septic arthritis most common cause in pediatrics and elderly.
4- pneumonia → most common cause of nosocomial pneumonia
5- scalded skin syndrome → Diffuse epidermal peeling that desquamates→exfoliatin
toxin.
6- toxic shock syndrome : Fever, hypotension, scarlatiniform rash (erythroderma)
that desquamates (particularly on palms and soles),diarrhea, multiorgan failure.
7- acute bacterial endocarditis
8- surgical infections →cellulitis or abscess
9- bacteremia
o Community
 Staphylococcal food poisoning
-2-4 huors after ingestion of heat stable toxin and last for day or two.
-salad dressings, sandwiches, meat products & cheese.
-Food handlers who have skin boils or eye infections.
-An intoxication (not an infection) of abrupt severe nausea, vomiting , cramps, and
prostration,often accompanied by diarrhea,hypotension and hypothermia.
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-Diagnosis by recovery of the organism or the toxin from food or either stool or
vomitus of infected persons.
o Pharma
Treatment
-Gastroenteritis is self-limiting.
-Nafcillin/oxacillin are drugs of choice because of resistance to penicillin due to
production of pencillinase enzyme →plasmid controlled.
-Methicillin is not used due to its toxicity.
-For methicillin-resistant Staphylococcus aureus (MRSA): vancomycin → resistance
mediated by gene mutations →change in penicillin binding proteins.
-For vancomycin-resistant Staphylococcus aureus (VRSA) or vancomycin intermediate
S. aureus (VISA)→plasmid controlled resistance: quinupristin/dalfopristin or
linezolid.
S.aureus key clues.
-Coagulase (+), gram (+) cocci in clusters
-Gastroenteritis: 2−6 h onset, salty foods, custards.
-Endocarditis: acute
-Toxic shock syndrome: desquamating
rash, fever, hypotension
- Impetigo: bullous
- Pneumonia: nosocomial.
-Osteomyelitis: #1 cause
2. Staphylococcus epidermis
-Coagulase (−); gram (+) cocci. -Novobiocin sensitive
-Infections of prosthesis and shunts (most common cause and almost exclusively
nosocomial)
-Capsule →virulence factor. -Treated by vancomycin.
3. Staphylococcus saprophyticus
-Coagulase (−), gram (+) cocci -Novobiocin resistant
-Second most common cause of community acquired UTI in sexually active females
“Honeymoon cystitis”.
 Genus : streptococcus
Key clues Group A Streptococcus
o Genus Features - Catalase (−), β hemolytic, bacitracin
-Gram-positive cocci in chains sensitive, gram (+) cocci
-Catalase negative -Pharyngitis: abrupt onset, tonsillar
-Serogrouped using known antibodies to the cell wall abscesses
Carbohydrates (Lancefield groups A–O) -Scarlet fever: blanching, sandpaper
rash, strawberry tongue
– S. pneumoniae serotyped via capsule -Impetigo: honey-crusted lesions
– S. pyogenes serotyped via M protein
1. Streptococcus pyogenes (Group A Streptococcus; GAS)

 Distinguishing Features
-β hemolytic
-Bacitracin sensitive
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 Pathogenesis
-M-protein: antiphagocytic
-Streptolysin O: immunogenic, hemolysin/cytolysin
-Streptolysin S: not immunogenic, hemolysin/cytolysin
-Spreading Factors:
-Streptokinase: breaks down fibrin clot
-Streptococcal DNAse: liquefies pus→extension of lesion.
-Hyaluronidase: hydrolyzes the ground substances of the connective tissues.
-Exotoxins A–C (pyrogenic or erythrogenic exotoxins) → Cause fever and rash of
scarlet fever → Superantigens.
-Antibodies to streptolysin O (ASO) titer of >200 is significant for rheumatic fever.
o Medicine
 Diseases :
1-erysipelas : painful red patches that enlarge and thicken resulting from
inflammation of the dermal layer of skin.
2-impetigo : honey(golden) crusted lesions over erythematous skin.
3-cellulitis (most common cause)
4-necrotizing fasciitis : acute pain and swelling at the site of the wound ,overlying
skin tightens becomes discolored, fever and confusion that may ultimately result in
shock and death.
*The above two diseases is usually the results of wound infections.
5- streptococcal pharyngitis → most common of strep. Infections. fever , sore throat,
tender cervical lymph nodes with enlargement of tonsils and visualization of
exudates.
 Post streptococcal complications:
1- acute glomerulonephritis
2- rheumatic fever:
-immune complex disease affecting connective tissue of joints , heart and brain.
-related to a previous group A-b hemolytic streptococcal infection of serotypes
(3,5,18,19,24).
-cross reaction between M protein in those serotypes and connective tissue of joints
, heart and brain.
- presentation is usually after few weeks of streptococcal pharyngitis with migratory
arthritis.
-diagnosis is usually based on the evidence of a preceeding streptococcal infection
with 2 major criteria or 1 major and 2 minor criteria
Major criteria → polyarthritis,carditis, erythema marginatum,subcutaneous nodues
and chorea.
Minor criteria → fever , arthralgia , prolonged PR interval, ↑CRP,↑ESR,↑WBC
-arhralgia and arthritis , carditis and prolonged PR , erythema marginatum and
subcut. Nodules cannot be used together for diagnosis.
-study well the clinical presentation it is easy but cannot be explained here.
Treatment :
-bed rest and monitoring.
-oral penicillin to eradicate streptococcal infection then long term prophylaxis.
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-for the acute attack use salicylates (aspirin) if the presentation is arthritis\carditis
without CHF.
-if carditis with CHF then prednisone.
- if chorea is the only isolated finding then Phenobarbital.
-patients with penicillin allergy should be prescribed erythromycin.
Complications :
-valvular heart disease (mitral\aortic\tricuspid), heart failure.
Prevention of recurrences:
-continuous antibiotic use→ one injection every 4 weeks.
-Discontinue after at least 5 years if doesn’t have carditis.
-If carditis then continue till adulthood or at last 10 years.
o Pediatrics
Scarlet fever
 Clinical course: After the acute onset of fever and sore throat, the rash appears 12
to 48 hrs. Abdominal pain ± vomiting are helpful diagnostic signs. The enanthem
consists of enlarged beefy red exudative tonsillitis, and a strawberry-resembling
tongue. The exanthem is a generalized intense orange-red eruption. Discrete linear
erythema in skin folds also has been noted in the patient with scaret fever called
Pastia’s lines. Desquamation happens during 1 to 3 weeks.
 Diagnosis and treatment: The diagnosis is mainly clinical. It may be confirmed with
throat culture and increasing antistreptolysin - O titer. Without antibiotic treatment,
the exanthem lasts four to five days, leaving a fine scale as it fades. Penicillin is the
drug of choice (oral or injectable).
2. Streptococcus agalactiae (Group B Streptococci; GBS)
Key clues S. agalactiae
o Distinguishing Features -Gram (+), catalase (−), B hemolytic,
-β hemolytic bacitracin resistant, CAMP test (+)
-Bacitracin resistant -Neonatal meningitis and
-Hydrolyze hippurate septicemia:
-CAMP test positive #1 cause, especially in prolonged
o Transmission: newborn infected during birth labors
(increased risk with prolonged labor after rupture of membranes)
o Diseases: neonatal septicemia and meningitis; most common causal agent
o Treatment: ampicillin with an aminoglycoside.
3. Streptococcus pneumoniae
-α hemolytic Key clues Streptococcus
-Optochin sensitive pneumoniae
-Lancet-shaped diplococci -Gram (+), catalase (−), hemolytic,
-Lysed by bile soluble in bile, optochin sensitive
-Pneumonia—typical, most common
o Predisposing Factors cause, rusty sputum
-Antecedent influenza or measles infection -Meningitis—many PMNs,
-Chronic obstructive pulmonary disease (COPD) glucose,
-Congestive heart failure (CHF) ↑protein in CSF, most common
-Alcoholism adult cause
-Asplenia predisposes to septicemia -Otitis media and sinusitis—most
common cause.
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o Pathogenesis
-Polysaccharide capsule is the major virulence factor
o Diseases
1- Typical pneumonia
− Most common cause of community acquired pneumonia,if nosocomial then Staph.
− Shaking chills, high fever, lobar consolidation, blood-tinged, “rusty”sputum
2-Adult meningitis
− Most common cause
− CSF reveals high WBCs (neutrophils) and low glucose, high protein
3-Otitis media and sinusitis in children →most common cause
o Treatment
-Bacterial pneumonia→macrolides or amoxicillin
-Adult meningitis→Ceftriaxone or cefotaxime (agents of choice in meningitis).
-Otitis media and sinusitis in children→amoxicillin
o Vaccine
s.pnemoniae has ≥80 serotypes according to the capsular polysaccharide antigen.
− Pediatric (PCV, pneumococcal conjugate vaccine)
-Thirteen of the most common serotypes
-Conjugated to diphtheria toxoid
-Prevents invasive disease
− Adult (PPV, pneumococcal polysaccharide vaccine)
-23 of the most common capsular serotypes
-Recommended for all adults ≥65 years of age and any at-risk individuals.
4. Viridans Streptococci
-α hemolytic
-Optochin resistant
-Pathogenesis→dextran (biofilm)−mediated adherence onto tooth enamel or
damaged heart valve and to each other (vegetation); growth in vegetation protects
organism from immune system.
o Diseases
Infective endocarditis (subacute)
− Malaise, fatigue, anorexia, night sweats, weight loss, splinter hemorrhages
− Predisposing conditions: damaged (or prosthetic) heart valve and dental
work without prophylactic antibiotics or extremely poor oral hygiene
o Treatment→penicillin G with aminoglycosides for endocarditis
o Prevention→prophylactic antibiotics prior to dental work for individuals with
damaged heart valve.
Key clues Viridans Streptococci
5. Enterococcus faecalis/faecium - Gram (+), , hemolytic, optochin resistant,
o Distinguishing Features bile insoluble

-Plaque and dental caries
-Group D gram-positive cocci in chains - Subacute bacterial endocarditis—preexisting
-PYR test positive damage to the heart valves; follows dental
work.
-varied hemolysis
-Hydrolyze esculin in 40% bile and 6.5% NaCl (bile esculin agar turns black)
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o Pathogenesis
-Bile/salt tolerance allows survival in bowel and gall bladder.
-During medical procedures on GI or GU tract: E. faecalis → bloodstream
→ previously damaged heart valves → endocarditis
o Diseases
-Urinary and biliary tract infections
-Infective (subacute) endocarditis→in persons (often elderly) with damaged
heart valves
o Treatement →vancomycin , for low resistant strains ampicillin
+aminoglycoside.
o Prevention→prophylactic use of penicillin and gentamicin in patients with
damaged heart valves prior to intestinal or urinary tract manipulations.
Key clues Enterococcus faecalis/faecium
Gram (+), catalase (−), variable
hemolysis, hydrolyzes esculin
Urinary/biliary tract infections—
elderly males
Subacute bacterial endocarditis—
elderly males, follows GI/GU surgery,
preexisting heart valve damage
Test youself part-1-
1- A 1-day-old newborn is evaluated for possible sepsis. Blood cultures grow gram-positive
cocci in pairs and chains that agglutinate with group B antiserum. The most likely
epidemiologic risk factor for this infection involves bacterial colonization of which of the
following?
(A) Mother's vagina
(B) Newborn's gastrointestinal tract
(C) Newborn's nasopharynx
(D) Placenta
(E) Umbilical cord remnant
Questions 2- 5 refer to the following case:
A 7 -year-old girl develops a sore throat, fever, and earache of approximately 1 week
duration. Upon examination by her physician, an erythematous rash is noted covering most
of her body and her tongue appears bright red.
2- Which of the following is the description of the causal agent?
(A) Gram-positive coccus, alpha hemolytic, catalase negative
(B) Gram-positive coccus, beta hemolytic, catalase negative
(C) Gram-positive coccus, alpha hemolytic, catalase positive
(D) Gram-positive coccus, beta hemolytic, catalase positive
(E) Gram-positive coccus, gamma hemolytic, catalase negative
3- The causal agent is identified by serotyping of the
(A) capsule(B) M proteins(C) outer membrane proteins(D) pili(E) teichoic acids
4-Past history includes a severe allergic reaction to amoxicillin when used for an ear
infection. The physician needs to treat this infection, but prefers not to use a drug that
needs parenteral administration.
Which one of the following agents is most likely to be appropriate in terms of both
effectiveness and safety? (answer this MCQ after studying all antibiotics)
A. Azithromycin B. Cefaclor C. Doxycycline D. Penicillin G E. Vancomycin
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5-All of the following are features of scarlet fever EXCEPT:

A.An erythematous, popular eruption with perioral pallor
B.Desquamation
C.pastia lines
D.Red strawberry tongue
E.Preauricular lymphadenopathy.
Question 6 refer to the following case:
6-A 71-year-old man is admitted from his extended care facility (nursing home)because of recent
aggravation of an exfoliative skin condition that has plagued him for several years. He had been
receiving a variety of topical antibiotic regimens over the last year or two. He now has a temperature
of 38.9°C (102°F). The skin of upper chest, extremities, and neck shows erythema with diffuse
epidermal peeling and many pustular lesions. Cultures obtained from these lesionswere reported
back from the laboratory as yielding a gram-positive organism that is highly salt (NaCl) tolerant.
What lab result is used to confirm the species of the causal agent?
(A) Bacitracin sensitivity
(B) Bile solubility
(C) Catalase production
(D) Coagulase production
(E) Optochin sensitivity
7-A 70-year-old woman is brought to the emergency department by her spouse with complaints of
shortness of breath and fever. Physical examination revealed a fever of 103°F, hypotension, and a
diastolic murmur. History revealed a cardiac valve replacement 5 years earlier. Three consecutive
blood cultures taken during febrile periods revealed gram-positive cocci that were catalase-positive
and coagulase-negative. Which of the following organisms is the most likely cause?
(A) Enterococcus faecalis
(B) Kingella kingae
(C) Staphylococcus aureus
(D) Staphylococcus epidermidis
(E) Staphylococcus saprophyticus
Question 8-9 refer to the following case:
8-A 65-year-old man develops pneumonia. The organisms isolated from the sputum are gram-positive
cocci that are alpha hemolytic on blood agar and sensitive to optochin. Which structure of the causal
agent provides protectionagainst phagocytosis?
(A) Capsule(B) Catalase (C ) Coagulase (D) M protein(E) Teichoic acid.
9-All of the following are predisposing conditions that increase the risk for development of
acute bacterial meningitis due to S pneumoniae EXCEPT:
A. Alcoholism
B. Pneumococcal pneumonia
C. Pneumococcal sinusitis
D. Pregnancy
E. Splenectomy
A 60-year-old woman is hospitalized following a stroke and develops a high grade fever with chills.
She is catheterized due to urinary incontinence andreceives cephalosporin for treatment of
pneumonia. Blood cultures and Gramstain are performed by the laboratory. The organisms isolated
are gram-positivecocci that are catalase-negative and capable of growth in 6.5% sodium chloride.
Which of the following is the most likely causal agent?
(A) Enterococcus faecalis
(B) Staphylococcus aureus
(C) Staphylococcus epidermidis
(D) Streptococcus pyogenes
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(E) Viridans streptococci

18-year-old previously healthy woman who presents with fever and hypotension. On the
morning of admission, she felt quite ill with fevers, rigors, nausea, vomiting, and diarrhea. As
the day progressed, she developed redness of her skin all over and became lethargic and
ultimately quite difficult to arouse. BP was noted to be 70/50 mmHg, with a HR of 140 bpm,
temperature of 39.5°C, and RR of 24 breaths/min. Oxygen saturation is 94% on room air. She
is minimally responsive. Skin examination reveals generalized erythroderma but no signs of
skin tears or infection. Genitourinary examination reveals a retained tampon that is
immediately removed. blood cultures are negative by 12 hours. You suspect staphylococcal
toxic shock syndrome (TSS). Which of the following statements regarding staphylococcal TSS
is true?
A. A skin site infection is clinically apparent in most cases.
B. Blood cultures will likely return positive by 24–36 hours given her grave clinical
presentation.
C. Desquamation of the skin will occur within 1–2 days.
D. High-dose IV penicillin should be started immediately.
E. It is caused by a toxin that binds to the invariant region of the major histocompatibility
complex and directly stimulates T-cell replication.
12)What is the most likely mechanism of resistance for methicillin-resistant staphylococcus

aureus to antistaph penicillins?
A. methylation of the binding site
B. active efflux of the drug from the bacteria
C. β-lactamase production
D. phosphorylation of the drug by bacterial enzymes
E. structural modifications of PBPs
Prepared by :
Haitham nabeel
Baghdad university-school of medicine.
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GRAM-NEGATIVE COCCI
 GENUS: NEISSERIA
o Genus Features
-Gram negative
-Diplococci with flattened sides
-Oxidase positive
1.Neisseria gonorrhoeae
o Micro
Distinguishing Features Key clues Neisseria gonorrhoeae
-Sexually active patient
-Gram-negative, kidney bean–shaped diplococcic
-Urethral/vaginal discharge (leukorrhea)
Pathogenesis -Arthritis possible
 Pili: -Neonatal ophthalmia
-Gram (−) diplococcus in neutrophils
– Attachment to mucosal surfaces
– Inhibit phagocytic uptake
– Antigenic (immunogenic) variation: >1 million variants
-Organism invades mucosal surfaces and causes inflammation.
 Culture (when done) on Thayer-Martin medium or chocolate agar (fastidious
microorganisims)
– Oxidase-positive colonies
– Maltose not fermented
– No capsule
o Medicine
 In men: Symptoms may occur within two to five days after exposure. However,
men may not develop noticeable symptoms for several weeks, and some may never
develop symptoms. A person is more likely to spread the infection to other partners
when symptoms remain “silent” like this.
-Symptoms: greater frequency or urgency of urination • a pus-like discharge from the penis
(white, yellow, or greenish) • swelling or redness at the opening of the penis • swelling or
pain in the testicles • a persistent sore throat.
 In women: symptoms may be more difficult to identify. Gonorrhea infection is often
mistaken for common vaginal yeast.
Symptoms : Discharge from the vagina • Pain or burning sensation while urinating • The
need to urinate more frequently • Sore throat • Pain upon engaging in sexual intercourse
• Sharp pain in the lower abdomen • Fever.
 Infants: ophthalmia (rapidly leads to blindness if untreated).
Case scenario\ A young woman developed a feverish illness with painful swelling of her
knee, elbow, and wrist joints. She has a sparse rash on the distal parts of her limbs,
consisting of small hemorrhagic pustules with an erythematous base. A smear was obtained
from the exudate of the exanthem and Gram stained. The stain showed intracellular gram-
negative diplococci.
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Disseminated gonorrhea : untreated gonorrhea →blood stream → rash, fever, or pain in
the joints may eventually develop.
Diagnosis :
1- Culture is the most common diagnostic test for gonorrhea. (the standard test for dx.)
2- DNA probe 3- The polymerase chain reaction (PCR) assay 4- ligand chain assay.
-When disseminated gonorrhea is suspected, blood and joint effusions should be sent for
Gram stain and culture. Negative Gram stain results and sterile cultures do not rule out
disseminated disease. The highest yield of N gonorrhoeae organisms in gonococcemia is
from mucosal sites, including the pharynx, urethra, cervix, or rectum. Urethral and cervical
cultures are typically the most revealing.
o Treatement : Ceftrtriaxone+ azithromycin or doxycycline for 14 days.
2.Neisseria meningitides
o Micro
Distinguishing Features
-Gram-negative, kidney bean–shaped diplococci
-Large capsule; latex particle agglutination →to identify N. meningitidis capsular antigens
in CSF
-Grows on chocolate (not blood) agar
-Ferments maltose in contrast to gonococci
Pathogenesis
 Important virulence factors:
-Polysaccharide capsule: antiphagocytic, antigenic, 5 common serogroups(A,B,C,Y,W135)
-Endotoxin (lipooligosaccharide): fever, septic shock in meningococcemia.
*Deficiency in late complement components (C5–C9) predisposes to bacteremia
Note: patients with ASPLENIA are at special risk of serious infection(especially meningitis)
with encapsulated bacteria (menigococci,pneumococci).
o Prevention
-Vaccine: capsular polysaccharide of 4 strains Y, W-135, C, and A.
o Pediatrics
 Meningiococcemia
Meningococcal disease is a global problem, the highest age-incidence of meningococcal
disease occurs in infants.
Clinical manifestations and spectrum:
 Occult meningococcal bacteremia
often manifests as fever with or without associated symptoms that suggest minor viral
infections. Resolution of bacteremia may occur without antibiotics, but sustained
bacteremia leads to meningitis in 60% of cases and to distant infection of other tissues.
 Acute meningococcemia :
pharyngitis, fever, weakness, vomiting, diarrhea, and/or headache. A maculopapular rash is
evident in some cases, with onset typically early in the course of infection. Limb pain,
myalgias, or refusal to walk occurs often. Cold hands or feet and abnormal skin color are also
early signs.
 In fulminant meningococcemia,
the disease progresses rapidly over several hours from fever without other signs to septic
shock characterized by prominent petechiae and purpura (purpura fulminans), hypotension,
DIC, acidosis, adrenal hemorrhage, renal failure, myocardial failure, and coma. Meningitis
may or may not be present.
 Meningococcal meningitis:
Headache, photophobia, lethargy, seizures, vomiting, nuchal rigidity, and other signs of
meningeal irritation are typically present.
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 Chronic meningococcemia:
fever, nontoxic appearance, arthralgias, headache, and a maculopapular to pustular rash,
often with a hemorrhagic component. Symptoms are intermittent, with a mean duration of
illness of 6-8 wk.
o Diagnosis:
-gram stain of blood or skin lesions may show gram negative diplococcic, definitive
diagnosis depends on isolation (culture)of menigiococci from blood , CSF or synovial fluid
but not from nasopharynx (not diagnostic) .cultures may be negative if antibiotic treatement
is started before collection. Detection of capsular polysaccharide antigens by rapid latex
agglutination tests in CSF can support the diagnosis in cases clinically consistent with
meningococcal disease but is not routinely recommended (false positive results).
o Treatment: Empirical therapy should be initiated immediately for possible invasive
meningococcal infections, B-lactams are the drugs of choice, penicillin or ampicillin
IV , Cephalosporin (Ceftriaxone or Cefotaxime) are acceptable alternatives. More
specific therapy for meningococcal disease may be initiated when culture and
antibiotic susceptibility results become available.
o Complications: Acute complications of severe meningococcal disease are related to
the vasculitis, DIC, and hypotension.
o Prognosis: Most deaths occur within 48 hr of hospitalization in children with
meningococcemia.
o Prevention: Antibiotic prophylaxis(rifampicin) is indicated for household, daycare,
and nursery school contacts and for anyone who has had contact with the patient’s
oral secretions during the 7 days before onset of illness.
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Test youself part-2-

1) 3 years old infant with one day history of fever that progressed rapidly to
repeated abnormal movements, loss of consciousness with diffuse bluish
discoloration of skin of both lower limbs. The most likely diagnosis is :
a- Meningiococcal meningitis b- sepsis c- meningococcemia d-tetanus
note: high fever + abnormal movements →think of febrile seizures.
2) 8 years old boy with history of fever and headache for the last few days, today he
developed visual disturbance with repeated seizures.
a- Meningiococcal meningitis b- sepsis c- meningococcemia d-tetanus
Questions 3-4 refer to the following case
Asexually active 23-year-old man with multiple sex partners has dysuria and a yellow
urethral exaudate .Gram stain of the exaudate shows numerous neutrophils ,many that
contain intracellular gram-negative diplococci. He has had three similar episodes of urethritis
over the past 2 years.
3) Which of the following properties 4) what is the drug of choice:
of the infecting organism best explains the a-penicillin
reinfection b-ciprofloxacin
A) pilli c- co-metrixazole
B) oxidase d-ceftriaxone
C) Inhibition of B-lymphocyte function
D) Inhibition of T-lymphocyte function
E) Polysaccharide capsule
5-All of the following serogroups are included in the quadrivalent meningococcus vaccine
EXCEPT:
A.A B.B C.C D.W135 E.Y
6-Which of the following is associated with a poorer prognosis for persons presenting with
meningococcal disease?
A.Presence of petechiae
B.Meningitis
C.Thrombocytosis
D.Leukocytosis
E.High ESR
7-Which of the following contacts should receive rifampin chemoprophylaxis after diagnosis
of invasive Neisseria meningitidis in a child?
A.All children and adults in the same household if there is an unimmunized or partially
immunized child younger than 48 mo
B.All children and adults in the same household or daycare facility regardless of
immunization history
C.All healthcare workers involved in care of the child, as well as household and daycare
contacts
D.Unimmunized or partially immunized children in the same household and in the same
daycare facility
E.All unimmunized or partially immunized healthcare workers involved in care of the child,
as well as unimmunized or partially immunized household contact.
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GRAM POSETIVE BACILLI

 GENUS: CORYNEBACTERIUM
o Genus Features
-Gram-positive rods
-Non−spore forming
-Aerobic
1-Corynebacterium diphtheria
o Micro
-Gray-to-black colonies of club-shaped gram-positive rods arranged in V or L shapes on
Gram stain→ chinese letter.
-When stained with methylene blue or albert stain →metachromatic granules
-Aerobic, non−spore forming
-Toxin-producing strains :The phage from one patient with diphtheria can infect the normal
nontoxigenic diphtheroid of another person and cause diphtheria
Pathogenesis
-Organism not invasive; colonizes epithelium of oropharynx or skin in cutaneous diphtheria.
-Diphtheria toxin (A-B component)—inhibits protein synthesis by adding ADP-ribose to
eEF-2→major virulence factor.
-Effect on oropharynx: Dirty gray pseudomembrane (made up of dead cells and fibrin
exudate, bacterial pigment)→the toxin is essential to form the pseudomembrane.
-Extension into larynx/trachea → obstruction
-Effect of systemic circulation of toxin → heart and nerve damage.
o Pediatrics
Diseases:
 Clinical Manifestations: The manifestations of C. diphtheriae infection are influenced by
the anatomic site of infection, and the production and systemic distribution of toxin.
Respiratory Tract Diphtheria
The primary focus of infection is the tonsils or pharynx, less commonly nose and larynx.
Incubation period is 2-4 days, In tonsillar and pharyngeal diphtheria, sore throat is the
universal early symptom while fever, dysphagia, hoarseness, malaise, or headache are less
common, This is followed by tonsillar membrane formation, which can extend to involve the
uvula, soft palate, posterior pharynx, or glottic areas. Underlying soft tissue edema and
enlarged lymph nodes can cause a bull-neck appearance. The degree of local extension
correlates directly with fatality due to airway compromise. The characteristic paucity of
other symptoms like fever and visualization of the membrane are important diagnostic
measures.
 Diagnosis Specimens for culture should be obtained from the nose and throat and any
other mucocutaneous lesion. A portion of membrane should be removed and submitted
for culture. The laboratory must be notified to use selective medium.
 Complications :
1-Respiratory tract obstruction by pseudo membranes.
2-systemic distribution of toxin which may cause
a- Toxic cardiomyopathy: Tachycardia, dysrhythmias and Heart failure are possible
manifestations. Recovery from the myocarditis is often slow but usually complete, it causes
50% of deaths.
b- Toxic Neuropathy : local manifestations like Paralysis of the soft palate, weakness of the
posterior pharyngeal, laryngeal, and facial nerves may follow, causing a nasal quality in the
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voice, dysphagia, and risk for aspiration,. Remote manifestations like Symmetric
polyneuropathy causes motor deficits with diminished deep tendon reflexes. Recovery is
often slow but usually complete.
Treatment and supportive care:
1- Specific antitoxin is the mainstay of therapy and should be administered on the basis of
clinical diagnosis.
2- . The role of antimicrobial therapy is to halt toxin production, treat localized infection, and
prevent transmission of the organism to contacts. Antibiotic therapy is not a substitute for
antitoxin therapy. drugs of choice are penicillin and erythromycin.
3- Bed rest is essential during the acute phase of disease, usually for ≥2 wk until the risk for
symptomatic cardiac damage has passed.
 GENUS: BACILLUS
o Genus Features
-Gram-positive rods
-Spore forming
-Aerobic
1-Bacillus anthracis
o Micro Bacillus anthracis
-Gram (+), spore forming, aerobic rods
-Contact with animal hides or postal
-Large, boxcar-like, gram-positive, spore-forming rods worker; eschar or life-threatening
-Capsule is polypeptide (poly-d-glutamate) pneumonia
-Potential biowarfare agent
o Transmission→ contact with infected animals or inhalation of spores (bioterrorism)
o Pathogenesis
-Capsule→polypeptide, antiphagocytic, immunogenic
- Anthrax toxin includes 3 protein components:
1-Protective antigen (B component)—mediates entry of LF or EF into eukaryotic cells
2- Lethal factor(LF)—kills cells
3- Edema factor(EF) →mediates edema
o Diseases
 Cutaneous anthrax: papule → papule with vesicles (malignant pustules)→ central
necrosis (eschar) with erythematous border often with painful regional
lymphadenopathy; fever in 50%→20%mortality
 Pulmonary (wool sorter’s disease)
− Life-threatening pneumonia; cough, fever, malaise, and ultimately facial edema , dyspnea,
diaphoresis, cyanosis, and shock with mediastinal hemorrhagic lymphadenitis→95%
mortality
 Gastrointestinal anthrax
− Rare
− Edema and blockage of gastrointestinal tract can occur, vomiting and bloody diarrhea,
hemorrhagic ascites, high mortality.
o Diagnosis
-Gram stain and culture of blood, respiratory secretions or lesions
-Serology
-PCR
o Treatment→penicillin (in the lecture),ciprofloxacin(in all other sources),
doxycycline(prophylactic).
o Prevention
-Toxoid vaccine →Given to individuals in high risk occupations
Bacillus cereus
-Rapid-onset gastroenteritis
-Fried rice, Chinese restaurants
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2-Bacillus cereus
o Pathogenesis:two possible toxins:
1-Emetic toxin (heat stable toxin): preformed fast (1–6 hours), similar to S. aureus with
vomiting and diarrhea; associated with fried rice
2-Diarrheal toxin(heat labile toxin) produced in vivo (meats, sauces): 18 hours, similar to E.
coli; → watery diarrhea.
o Community
-disease is either emetic or diarrheal lasting no more than 24 hrs . diagnosis →clinical can be
confirmed with suspected food culture.
-outbreak of emetic type have been most commonly associated with cooked rice.
-preventive measures→ foods should not remain at ambient temperature after cooking.
 GENUS: CLOSTRIDIUM
o Genus Features
-Gram-positive rods
-Spore forming
-Anaerobic
1-Clostridium botulinum Clostridium botulinum
o Micro -Home-canned alkaline vegetables
Distinguishing Features -Floppy baby syndrome (infant with

flaccid paralysis)
-Anaerobic -Reversible flaccid paralysis
-Gram-positive spore-forming rods
o Transmission→ foodborne/traumatic implantation.
o Pathogenesis
 Spores survive in soil and dust; germinate in moist, warm, nutritious but anaerobic
conditions
 Botulinum toxin
− A-B polypeptide neurotoxin (actually a series of 7 antigenically different; type A and B
most common)
− Coded for by a prophage (lysogenized Clostridium botulinum).
− Highly toxic
− Heat labile (unlike staph), 20 minutes 100.0°C
− Mechanism of action
-Absorbed by gut and carried by blood to peripheral nerve synapses
-Blocks release of acetylcholine at the myoneuronal junction resulting in a reversible flaccid
paralysis.
o Medicine
 Adult botulism :
Clinical presentation :
-Nausea, vomiting, diarrhea ,Cranial nerve involvement, which almost always marks the,
onset of symptoms, usually produces Double vision, Difficulty speaking or swallowing,
Descending Symmetrical flaccid paralysis , Respiratory muscle paralysis, Paralytic ileus,
severe constipation, urinary retention are common, Ptosis is frequent; the pupillary reflexes
may be depressed ,fixed or dilated pupils are noted in half of patients., The gag reflex may
be suppressed.
-Patients do not have fever , sensory findings. Patients are alert and oriented with intact
deep tendon reflexes.
 Infant botulism :
-Most common form in U.S. , Spores from varied sources → Honey, corn syrup .
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-Clinical signs: Constipation ,Lethargy, Poor feeding, Weak cry, Bulbar palsies, Failure to
thrive.
 Diagnosis : A diagnosis of botulism is clinical and must be considered in patients with
symmetric descending paralysis who are afebrile and mentally intact.
o Treatement: -intensive care immediately → Patients should be hospitalized and
monitored closely for incipient respiratory failure.
-equine antitoxin should be administered as soon as possible, Antibiotic therapy does not
affect the course of illness.
o Community
There are 3 forms of botulism→ 1- foodborne (classic form ) 2- wound 3- intestinal
botulinum .
-the foodborne is caused by preformed toxins.
-toxin is produced in canned , alkaline foods.
-infant botulism Is caused by ingestion of honey contaminated with spores.
-intestinal form means ingestion of spores not preformed toxins.
o Prevention :
- Proper canning; heat all canned Foods.
-No honey first year.
2-Clostridium tetani
o Micro
-Large gram-positive, spore-forming rods ,terminal spores →drumstick apearance
-Anaerobes
-Produces tetanus toxin
o Transmission→ Puncture wounds/trauma (human bites).
o Pathogenesis
-Spores germinate in the tissues, producing tetanus toxin (an exotoxin also called
tetanospasmin).
-Carried intra-axonally to CNS, also may spread via blood.
-Binds to ganglioside receptors
-Blocks release of inhibitory mediators (glycine and GABA) at spinal synapses
-Excitatory neurons are unopposed → extreme muscle spasm
-One of the most toxic substances known.
o Pediatrics
Clinical presentation : The presenting symptom in about half of cases is trismus, This
followed by stiffness, difficulty chewing, dysphagia, and neck muscle spasm. The sardonic
smile of tetanus (risus sardonicus) results from intractable spasms of facial and buccal
muscles, the patient may assume an arched posture of extreme hyperextension of the body,
or opisthotonos, Laryngeal and respiratory muscle spasm can lead to airway obstruction.
patient remains conscious, in extreme pain, and in fearful anticipation of the next tetanic
seizure, Fever, occasionally as high as 40°C, is common, The tetanic paralysis becomes
severe in the 1st wk after onset, stabilizes in the 2nd wk, and ameliorates over the ensuing
1-4 wk.
Neonatal tetanus The infantile form of generalized tetanus, typically manifests within 3-12
days of birth as progressive difficulty in feeding (sucking and swallowing), associated hunger,
and crying. Paralysis or diminished movement, stiffness and rigidity to the touch, and
spasms, with or without opisthotonos, are characteristic.
Diagnosis: clinical mainly. C. tetani is not always visible on Gram stain of wound material.
The umbilical stump may hold remnants of dirt, dung, clotted blood, or serum, or it may
appear relatively benign.
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Management: goals are eradication of c.tet, neutralization of toxin , control seizures and
prevention of recurrences.
1-TIG should be given as soon as possible in order to neutralize toxin that diffuses from the
wound into the circulation before the toxin can bind at distant muscle groups.
2-antibiotics → Penicillin G (100,000 U/kg/day IV for 10-14 days) .
3- All patients with generalized tetanus need muscle relaxants→ Diazepam
4- the patient should be sedated and protected from all unnecessary sounds and touch.
Complications and prognosis: aspiration of secretions and pneumonia may be apparent. The
most important factor that influences outcome is the quality of supportive care. Mortality is
highest in the very young and the very old.
o Medicine
Symptoms:
1-generalized tetanus : incubation ranges from 4 to 14 days, Patients may report a sore
throat with dysphagia (early sign) stiffness, neck rigidity, restlessness, and reflex spasms.
Other early features include, diaphoresis, and with hydrophobia, drooling, and spasm of the
back muscles. Muscle rigidity spreads in a descending pattern from the jaw and facial
muscles over the next 24-48 hours to the extensor muscles of the limbs. Reflex spasms
develop in most patients and can be triggered by minimal external stimuli such as noise,
light, or touch. the patient does not lose consciousness and usually experiences severe pain.
Late in the disease autonomic dysfunction develops include elevated temperature, sweating,
elevated blood pressure, and episodic rapid heart rate.
2-localized tetanus : Localized tetanus involves an extremity with a contaminated wound
and is of highly variable severity. It is an unusual form of tetanus, and the prognosis for
survival is excellent.
3-cephalic tetanus : Cephalic tetanus generally follows head injury or develops with infection
of the middle ear. Symptoms consist of isolated or combined dysfunction of the cranial
motor nerves (most frequently CN VII). Cephalic tetanus may remain localized or may
progress to generalized tetanus. It is an unusual form of tetanus with an incubation period
of 1-2 days. The prognosis for survival is usually poor.
4- neonatal tetanus : The usual cause is the use of contaminated materials to sever or dress
the umbilical cord in newborns of unimmunized mothers. The newborn usually exhibits
irritability, poor feeding, rigidity, facial grimacing, and severe spasms with touch. Mortality
exceeds 70%.
Complications : sudden cardiac death has become the leading cause of death. Sympathetic
overactivity is the major cause of tetanus-related death in the intensive care unit (ICU).
asphyxia from tetanic spasms was(previously) the usual cause of death in patients with
tetanus. Nosocomial infections, Long bone fractures, joint dislocations, aspiration
pneumonia.
Diagnosis : The diagnosis of tetanus is based on clinical findings.
o Treatment :1- Wound management → All patients with tetanus should undergo
wound debridement.2- Antimicrobial therapy →plays a minor role (with penicillin or
metrinedazole) 3- The toxin is neutralized with shots of tetanus immune globulin
4- Active immunization
3-Clostridium perfringens
o Micro
-Large gram-positive, spore-forming rods (spores rare in tissue), nonmotile
-Anaerobic:
-Reservoir→soil and human colon
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o Transmission→ foodborne and traumatic implantation
o Pathogenesis
 Spores germinate under anaerobic conditions in tissue.
 Vegetative cells produce:
-Alpha toxin (phospholipase C) is a lecithinase. It disrupts membranes ,damaging RBCs,
platelets, WBCs, endothelial cells → massive hemolysis, tissue destruction, hepatic toxicity.
- Enterotoxin produced in intestines in food poisoning: disrupts ion transport→ watery
diarrhea, cramps (similar to E. coli); resolution <24 hours.
o Surgery
Gas gangrene (primary gangrene) : It is a deadly form of gangrene, The organisms produce
edema and gas in the affected tissues, Infection spreads rapidly as the gases produced by
bacteria expand and affect healthy tissue. Gas gangrene can cause necrosis, gas production,
and sepsis. Progression to toxemia and shock is often very rapid. gas gangrene should be
treated as a medical emergency.
o Community
-it is sometimes called the cafeteria poisoning. IP →10-12 hrs. Intestinal disorder
characterized by intestinal colic and diarrhea. resolution <24 hours. Diagnosis by recovery of
organisims in culture or detection of toxin. Caused by type A strains. All outbreaks are
associated with in adequate heating or re heated meats.it is a non inflammatory diarrhea.
-Severe disease causing necrotizing enteritis are caused by type C strains.
4-Clostridium difficile
-Reservoir—human colon/gastrointestinal tract
o Transmission—endogenous
o Disease(s)—antibiotic-associated (clindamycin, cephalosporins) diarrhea, colitis, or
pseudomembranous colitis (yellow plaques on colon)
o Treatment
-Severe disease→ metronidazole: if resistant then vancomycin.
-Mild disease→ discontinue other antibiotic therapy.
*From those 2 lines was 2 final mcqs and one mid exam mcq in our year.
Test yourself part-3

Case scenario for question 1
1)A 6-year-old girl had crashed on a toboggan ride and complained of pain in the perineal area. Exam
showed only bruising of the area. Two days later, she develops fever, prostration, discoloration of the
buttock, and blebs of the skin in the area. After admission to the hospital, she develops progressive
involvement of the leg, thigh, and buttock with extension to the lower abdomen. She goes into shock
and dies before surgery could be performed. At autopsy, a 1-inch piece of wood is found in the
perineum, which had perforated the anus. The most likely causal agent:
(A) requires an elevated oxidation reduction potential
(B) is a gram-negative coccobacillus
(C) is a marked lecithinase producer
(D) is non hemolytic on blood agar
(E) is non fermentative
2)What is the typical means of transmission of a toxin that blocks the release of inhibitory
transmitters GABA and glycine?
(A) Eating home-canned foods
(B) Fecal-oral, travel to foreign country
(C) Infant given honey during the first year of life
(D) Puncture wound
(E) Respiratory, with incomplete vaccination history
Case scenario for question 3-4-5
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A 10-year-old girl with an incomplete vaccination history presents to her pediatrician with a fever of
101.5°F, sore throat, malaise, and difficulty breathing. Physical examination reveals cervical
lymphadenopathy and a gray, leathery exudate in the rear of the oropharynx. The area bleeds
profusely when disturbed with a tongue depressor.
3)Which of the following correctly describes the causal agent?
(A) Gram-negative rod; toxin that inhibits protein synthesis
(B) Gram-negative rod; toxin that increases cAMP
(C) Gram-positive aerobic rod; toxin that inhibits protein synthesis
(D) Gram-positive anaerobic rod; toxin that inhibits protein synthesis
(E) Gram-positive aerobic rod; toxin that increases cAMP
4)The patient is at risk for which of the following complications of this disease
A. Epidural abscess B. Hepatitis C. Meningitis D. Myocarditis E. Rheumatic fever
5)Regarding her management , all are true except:
a)order the laboratory to use specific culture media
b)the antibiotics of choice are penicillin or erythromycin
c) patient should be monitored for possible airway obstruction.
d)antitoxin is given after laboratory confirmation
e)give antibiotic prophylaxis for household contacts even if they are vaccinated.
Case scenario for question 6-7-8-9
Two days after eating a meal that included home-canned green beans, 3 people developed various
degrees of visual problems, including double vision and difficulties focusing.
6)Describe the Gram reaction of the organism most likely to be isolated from the leftover beans and
lab findings which would be used in its identification: .
(A) A gram-positive coccus which is catalase-positive and grows in a high salt environment
(B) A gram-positive aerobic bacillus which sporulates
(C) A gram-positive coccus which is catalase-negative and optochin-resistant
(D) A gram-positive bacillus grown on a low oxidation-reduction medium
(E) A gram-negative bacillus capable of reducing nitrates to nitrites
7)What is the mechanism of action of the toxin?
(A) ADP ribosylation of eukaryotic elongation factor 2 (eEF-2)
(B) ADP ribosylation of Gi
(C) ADP ribosylation of GTP-binding protein
(D) Blocks release of acetylcholine
(E) Blocks release of inhibitory transmitters GABA and glycine
8)Regarding their illness , all the following is TRUE except:
a-it is not associated with fever.
b-caused by ingestion of spores
c-antitoxin is the mainstay of therapy
d-affects the motor system only
e-antibiotics plays no role at all in management
9)Patients are least likely to have ?
a-diminished tendon reflexes b-diminished pupillary reflexes c-urinary retention d- dyspnea

A 70-year-old man is hospitalized for an infection and treated with clindamycin .The patient improves
and returns to his nursing home. Two weeks later he is rushed to the emergency room with fever and
loose, mucoid green stools. The diarrhea is voluminous, and he is having severe abdominal pain.
Sigmoidoscopy of his colon reveals yellow-white plaques.
10)What is the single most likely event/factor that contributed to this patient’s current illness?
(A) Administration of antibiotics
(B) Advanced age
(C) Drinking unpasteurized milk
(D) Eating contaminated cold cuts
(E) Living in nursing home
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Today, two adults present only hours apart to the emergency department with remarkably similar
cases. Both had attended a pig feast yesterday and awoke today with excruciating abdominal pain.
Both CT scans show extensive necrosis of the intestinal wall, most severely in the jejunum. The
causative organism of these infections is also most commonly causative in cases of which of the
following? A)Cellulitis B)Gas gangrene myonecrosis C) Meningitis D)Pharyngitis E)Pneumonia.
12)Which of the following antibiotics has the strongest association with the development of
C difcile–associated disease?
A)Ceftriaxone B)Ciprofoxacin C)Clindamycin D)Moxifoxacin E) Piperacillin-tazobactam
13)A 2 mo old child is seen in your clinic for the first time. The child was born at home, and
this is the 1st well-child visit. Risk factors for infant botulism that should be communicated
to the parents include:
A.Gardening
B.Home construction
C.Frozen vegetables
D.Honey
E.None of the above
A 64-year-old man with a long history of heroin abuse is brought to the hospital because of
fever and worsening muscle spasms and pain over the last day On examination, he is
extremely sweaty and febrile to 101.4°F. There are widespread muscle spasms including of
the face. He is unable to open his jaw due to muscle spasm and has severe back pain due to
diffuse spasm. On his leg, there is a skin wound that is tender and erythematous
Which of the following is true regarding the etiologic agent responsible for this infant’s
severe illness?
A. At the time of initial clinical presentation, death is most commonly due to cardiovascular
complications with this disease.
B. Blood cultures will yield gram-positive rods.
C. Diagnosis of this illness requires laboratory confirmation of the causative organism.
D. Permanent muscle dysfunction is likely after recovery
E. Wound cultures will be positive in approximately 20% of cases
Prepared by :
Haitham nabeel
Baghdad university-school of medicine
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GRAM NEGATIVE BACILLI

 FAMILY: ENTEROBACTERIACEAE(E.coli , klebsiella, salmonella, shigella, proteus)
o Family Features
-Gram-negative rods
-Facultative anaerobes
-oxidase negative
-Reduce nitrates to nitrites
o Family Pathogenesis
 Endotoxin
 Some also produce exotoxins.
 Antigens
–O= cell envelope or O antigen→ cell wall lipopolysaccharide
– H= flagellar (motile cells only) antigen
− K = capsular polysaccharide antigen
– Vi (virulence) = Salmonella capsular antigen
Lactose Fermenters Non−Lactose Fermenters
Mnemonic: ShYPS
Escherichia
Klebsiella
Nonmotile, Motile,
non-H2S producers H2S producers
Shigella Proteus
Yersina Salmonella
1-Escherichia coli
-Gram-negative rod.
-Facultative anaerobic, oxidase negative.
-E. coli is a lactose fermenter.
o Transmission
-Endogenous
-Fecal-oral(most common)
-Maternal fecal flora
-Enterohemorrhagic strains: bovine fecal contamination(undercooked hamburger).
PITcH.
EPEC→ P = pediatric
EIEC→ I = inflammatory
ETEC→ T = traveler
C = coli
EHEC→ H = hamburger
o Notes :
- most of E.coli species have O and H antigens (motile) but not K (non capsulated),all
antigens are heat stable and typing is based on those antigens.
- E.COLI is the most common cause of gram neg. sepsis most commonly in hospitalized
patients.
-In EHEC the disease may begin as watery then turns into bloody diarrhea but it is non-
inflammatory diarrhea (toxin), so no PMNs or fever that accompanies EIEC.
-mechanisms of pathogenesis and treatement in the below table which are not mentioned in
the lecture are for your knowledge only.
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Trans- Mechanism of Clinical Clues Treatment

mission Pathogenesis
1- UTI (most Endogenous Motility Gram (−) bacilli, Fluoroquinolone

common cause) fecal flora Adherence to ≥105 CFU/ml or sulfonamides
contaminae uroepithelium
and ascend
2- Neonatal Maternal Capsule, Blood, CSF Ceftriaxone
septicemia/ fecal flora endotoxin culture,
meningitis (2nd contaminae gram (−) bacilli
most common during
cause) parturition
3-Septicemia Indwelling IV Endotoxin Blood culture, Fluoroquinolones,
lines, gram (−) bacilli, third-generation
cytotoxic oxidase (−) cephalosporins
drugs
damage
intestinal
mucosa,
allow escape
4- ETEC Fecal/oral LT:heat-labile Noninflamma- Rehydration
(travelers’ toxin stimulates tory diarrhea
diarrhea) adenylate
cyclase by ADP
ribosylation of Gs
ST:stimulates
guanylate cyclase;
5- EPEC (second Fecal/oral Adherence to M Noninflamma- Beta-lactams
most common cells tory diarrhea in
infantile babies in
diarrhea) developing
countries
6-EIEC Fecal/oral Invades large Inflammatory
bowel diarrhea, blood,
Inflammatory pus, fever,
diarrhea; similar abdominal pain
to shigellosis
7- EHEC Bovine feces Verotoxin:Shigella- No fever, no Antibiotics ↑ risk
(VTEC):O157:H7 like toxins 1 and 2, PMNs, blood in of HUS
most common ↓ protein stool,; may
synthesis by progress to
interfering with hemorrhagic
60S ribosomal colitis and HUS;
subunit most common in
children <5
years
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Definition of abbreviations:; EIEC, enteroinvasive E. coli; EHEC, enterohemorrhagic E. coli;
EPEC, enteropathogenic E. coli; HUS, hemolytic uremic syndrome
2-Klebsiella pneumoniae
Klebsiella pneumonia key clues
o Micro -Elderly patient with typical pneumonia:
Distinguishing Features currant-jelly sputum
-Gram-negative rods with large polysaccharide capsule -UTI (catheter associated)
-Mucoid, lactose-fermenting colonies on MacConkey agar -Septicemia: immunocompromised or
-Oxidase negative nosocomial
o Transmission—endogenous -Gram (−) bacilli, oxidase (–),
o Pathogenesis encapsulated, lactose fermenters
-Capsule: impedes phagocytosis
-Endotoxin: causes fever, inflammation, and shock (septicemia)
Diseases:
 Pneumonia
– Community-acquired, most often in older males; most commonly in patients with either
chronic lung disease, alcoholism, or diabetes (but this is not the most common cause of
pneumonia in alcoholics;S. pneumoniae is.)
–Frequent abscesses make it hard to treat; fatality rate high.
– Sputum is generally thick and bloody (currant jelly) but not foul smelling as in anaerobic
aspiration pneumonia.
 Urinary tract infections—catheter-related (nosocomial) from fecal contamination
of catheters
 Septicemia—in immunocompromised patients, may originate from bowel defects or
invasion of IV lines
o Treatment
-Third-generation cephalosporin with or without an aminoglycoside
-Fluoroquinolones may also be used.
 GENUS: PROTEUS
o Genus Features
-Gram-negative rod
-Enterobacteriaceae(means they have the general characteristics of this family)
-Peritrichous flagella/highly motile/“swarming motility”
-Non–lactose-fermenting
-Urease positive
o Species of Medical Importance
-Proteus mirabilis (90% of infections) Proteus mirabilis/Proteus vulgaris
-Proteus vulgaris -Patient with UTI or septicemia
-Swarming motility
-Staghorn renal calculi (struvite stones)
3-Proteus mirabilis/Proteus vulgaris
-Gram (−), non−lactose fermenting,
o Distinguishing Features urease(+).
-Gram-negative rods
-Highly motile; “swarming” motility on surface of blood agar.
-Urease produced
-Facultative anaerobe (Enterobacteriaceae), oxidase negative
-produce H2S (remember the mnemonic SHYPS)
Note : Weil-Felix test: antigens of OX strains of Proteus vulgaris cross-react with rickettsial
organisms.
o Pathogenesis
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-Urease raises urine pH to cause kidney stones (staghorn renal calculi composed of
magnesium ammonium phosphate (struvite stones))
-Motility may aid entry into bladder→ UTI.
-Endotoxin causes fever and shock when septicemia occurs.
o Disease(s)
-Urinary tract infections
-Septicemia
o Treatment
-Fluoroquinolones, TMP-SMX, or third-generation cephalosporin for uncomplicated UTIs
.
 GENUS: PSEUDOMONAS
Key clues Pseudomonas
o Genus Features
-Gram-negative rod -Gram (−), oxidase (+), aerobic bacillus
-Oxidase-positive -Blue-green pigments, fruity odor
-Aerobic (non fermenting) -Burn infections—blue-green pus,fruity
Species of Medical Importance—Pseudomonas aeruginosa odor
Pseudomonas aeruginosa
-Typical pneumonia—cystic fibrosis.
-Oxidase-positive, Gram-negative rods, non fermenting -UTI—catheterized patients.
-Pigments: pyocyanin (blue-green) and fluorescein (pyoverdin)→ green-yellow.
-Grape-like odor
-Slime layer(glycocalyx)→mucoid colonies.
-Non–lactose fermenting colonies on MacConkey.
o Transmission—water aerosols, raw vegetables, flowers
o Pathogenesis
-Endotoxin causes inflammation in tissues and gram-negative shock in septicemia.
-Pseudomonas exotoxin A: ADP ribosylates eEF-2, inhibiting protein synthesis (like
diphtheria toxin)
-enzymes like elastase and proteases.
-Capsule/slime layer: allows formation of pulmonary microcolonies; difficult to remove by
phagocytosis and also the pigments→ damage cilia.
o Disease(s)
 Healthy people
– Transient gastrointestinal tract colonization: loose stools (10% population)
– Hot tub folliculitis
– Eye ulcers: trauma, coma, or prolonged contact wear→ corneal infection.
 Burn patients→ colonization of eschar →cellulitis (blue-green pus) → septicemia.
 Neutropenic patients
– Pneumonia and septicemias—often superinfections (infections while on antibiotics).
 Otitis externa
– Swimmers, diabetics, those with pierced ears.
 Septicemias
– Fever, shock with or without skin lesions (black, necrotic center, erythematous margin,
ecthyma gangrenosum).
 Catheterized patients
– Urinary tract infections (UTIs) → nosocomial.
 Cystic fibrosis
– Early pulmonary colonization, recurrent pneumonias.
-most common cause of gram neg. nosocomial pneumonia.
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o Treatment antipseudomonal penicillin(piperacillin) and an
aminoglycoside(tobramycinor gentamycin).
o Urinay tract infections.

-E.coli is the most common cause of UTI both in community and hospital setting.
- s.saprophyticus is the second most common cause of community acquired UTI especially in
sexually acquired females …. Remember (honey moon cystitis)
-pseudomonas is acquired in a hospital setting and is usually drug resistant.
-lower UTI →cystitis. Upper UTI→pyelonephritis.
-patients may present with a variety of manifestations including dysuria,urgency, frequency,
pyuria,hematuria.
-patients with pyelonephritis may have fever, chills, nausea and vomiting , CVA tenderness
and back pain.
-pyuria →pus cells (PMNs) in urine. Indicates urinary tract inflammation. Not specific for UTI.
-sterile pyuria → pyuria + failure of bacterial growth on culture media. Causes
are→antibitoc administration ,urethritis due to gonococci ,renal TB , urethritis due to
Chlamydia,trichomonas or viruses.
-asymptomatic bacteriuria →bacteria can be isolated in culture without causing symptoms→
do not need treatement except DM , elderly , pregnancy because if pregnant woman
developed pyelonephritis → low birth weight and prematurity.
Treatement :
-Uncomplicated UTI → trimethoprim-sulfamethoxazole for 3 days.
-Complicated UTI (UTI that has a high chance of not being adequatley cured or can recur like
if caused by resistant bacteria or accompanied by structural or functional abnormality in the
urinary tract )→floruoquinoles (ciprofloxacin) if gram neg. , ampicillin + gentamycin if pos.
Asymptomatic bacteruria in pregnancy→ amoxicillin , cephalexin.
 GENUS: SALMONELLA
o Genus Features
-Gram-negative rods (Enterobacteriaceae)
-Non–lactose fermenters
-Motile
4-Salmonella typhi
-Gram-negative rods, highly motile with the Vi capsule
-Facultative anaerobe, non–lactose fermenting
-Produces H2S
-Species identification with biochemical reactions
-when ferments glucose and mannose (not lactose)→it produces only acid without gas.
-Survive freezing in water for long period
o Antigenic structure
1-Somatic O-Ag→lipopolysacchride →heat stable.
2-Flagellar H-Ag→biphasic →heat labile.
Capsular Ag (Vi-Ag) –acidic polysaccharide layer covering cell wall, also heat-labile.
o Transmission
-human to human only.
-Fecal-oral route from human carriers (gall bladder)
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-Decreased stomach acid or impairment of mononuclear cells such as in sickle cell disease
predisposes to Salmonella infections.
o Pathogenesis
Large infecting dose because salmonella is sensitive to acid, Infection start in small
intestine multiply in peyers patches→ Salmonella reach basolateral side of M cells, then
mesenteric lymph nodes and blood. Liver and spleen are infected with additional release of
bacteria to bloodstream→ S. typhi survives intracellularly and replicates in macrophages;
resistant to macrophage killing ,Released from the macrophages; the Vi capsular antigen (S.
typhi only) withstands complement-mediated killing →Biliary system (liver, gallbladder) is
infected, organisms enter intestinal tract in bile.
o Clinical presentation
-The most prominent symptom is high and prolonged fever (38.8 to 40.5C), A prodrome of
nonspecific symptoms often precedes fever.
First week of typhoid : Increasing Fever • Headache • Myalgia • Relative bradycardia
• Constipation • Diarrhoea and vomiting in children.
-At the end of 1st week and second week : •Fever • Rose spots on trunk •Splenomegaly
• Cough •Abdominal distension/pain • Diarrhoea
-End of 2nd week • Delirium, complications, then coma and death (if untreated).
-Physical examination may reveal • Rash “rose spots” • Hepatosplenomegaly • Epistaxis • a
relative bradycardia.
o Diagnosis
1-Non specific tests→ WBC • Normal in majority. • Leukopenia in 25% of cases.
• Leukocytosis in children and if disease is complicated.
2-Specific tests
-Blood culture is the (most important diagnostic method).→ often positive from the 1st
week in enteric fever.
-Stool specimens positive in 2nd-3 rd weeks.
-urine cultures may be positive after a second week.
-Biopsy from rose spots, bone marrow. Intestinal aspirate → in carrier state .
-Widal test →Serum agglutinating( Abs) rise sharply during 2nd – 3rd weeks of typhoid
fever.
Results of Widal test
-Anti – O: appear 2nd – 3 rd week & stay for few weeks (>160)→recent infection.
-Anti-H: remain high (>160) reflecting old infection or immunization.
-Presence of anti-Vi occurs in carriers.
o Treatement
-The fluoroquinolones are the drugs of choice→ ciprofloxacin.
-ceftriaxone and cefotaxime are useful alternatives.
-Chronic carriers treated for 4 weeks with ciprofloxacin→Cholecystectomy may be necessary
-Duration of treatement is 14 days.
-Even with therapy, there is still a danger of: Complications. Relapse. Carrier state.
o Carriers : develop in about 5% of patients due to invasion of gall bladder causing
excretion of the bacteria in the feces, Carrier state higher among: • Women • Biliary
abnormalities (e.g. gallstones, GIT carcinoma) • Urinary stones • Schistosoma
haematobium.
o Complications : 1. Intestinal perforation and/or 2. Gastrointestinal hemorrhage. Can
develop despite clinical Improvement→ require immediate medical and surgical
interventions.
o Relapse : may occur 2-3 weeks after recovery.
S. enteritidis
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-Facultative gram-negative rods, non–lactose-fermenting on MacConkey medium
-Produces H2S, motile (unlike Shigella)
o pathogenesis
-Sensitive to stomach acid (infectious dose 10^5 organisms)→Lowered stomach acidity
(antacids or gastrectomy) increases risk.
-Invasion of epithelial & subepithelial tissues of S.I & L.I. organisms penetrate through the
mucosal cells into lamina propria  inflammation.
-May Spread to septicemia most commonly with→ S. enterica subsp. Choleraesuis.
o Community
 Food poisoning (salmonellosis)
-Mode of transmission : Ingestion of the organisms in food from infected animals or
contaminated by feces of an infected animal or person. This includes eggs, raw milk,
contaminated water, meat & poultry. The incidence rate of infection is highest in infants
and young children person-to-person spread can also occur.
-Manifestations : Acute enterocolitis, headache, abdominal pain, diarrhea,
nausea and sometimes vomiting. dehydration which may be severe and fever(invasive
diarrhea). A temporary carrier state occasionally continues for months, especially in infants
susceptibility Increased by: Achlorhydria, antacid treatment, gastrointestinal surgery,
broad-spectrum antibiotherapy, neoplastic disease, immunosuppressive treatment and
other debilitating conditions including malnutrition.
 GENUS: SHIGELLA
o Genus Features
-Gram-negative rod l Enterobacteriaceae
-Non–lactose fermenters but ferment other sugars producing acid only
-Nonmotile
o Species of Medical Importance(classified according to their biochemical &
serological criteria)
-Shigella sonnei (most common in U.S.)
-Shigella flexneri
-Shigella dysenteriae (most severe disease)
- Shigella boydii
5-Shigella Species
-Gram-negative rods, non motile,non capsulated→simply means they have no H or K antigen
-can not grow on simple media
-Antigenic structure :The somatic O Ag→ their serologic specificity depends on it.
o Transmission→fecal-oral spread
o Pathogenesis
-The most important and essential factor in shigella pathogenesis is its ability to invade.
It invades mucosal epithelial cells of large intestine and terminal ileum by induce
phagocytosis , micro-organisms multiply within the cytoplasm and pass to adjacent cells
microabscesses of the wall necrosis, superficial ulceration, bleeding and
pseudomembrane formation. The lesion heal by granulation and scar. it rarely causes
invasion of blood vessels.
-Shigella produces two important toxin.
-Endotoxin triggers inflammation
 Shiga toxin: also produced by enterohemorrhagic E.coli.
– Produced by S. dysenteriae, type 1 – Three activities: neurotoxic, cytotoxic, enterotoxic
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– AB component toxin is internalized in human cells; inhibits protein synthesis.
The story of this toxin : shiga or vero toxin inhibit protein synthesis inside its target cells
causing cell death. It kills the enterocytes reaching the blood , in the blood it has receptors
on the renal tubular cells → kills them causing acute renal failure , it also has receptors on
the endothelial cells causing platelets to adhere to damaged epithelium →
thrombocytopenia + if RBCs pass in these blood vessels they become distorted and lyse
→anemia. That’s why it causes hemolytic uremic syndrome.
o Medicine
 Clinical manifestations:
-Infections due to S. sonnei or S. boydii typically present after an incubation period of 1 to 3
days with fever and mild to moderate watery diarrhea . They do not cause serious
dehydration and resolve without treatment in 3 to 5 days. many white and red blood cells
are visible in stool examination indicative of the underlying inflammation of the mucosa.
S. flexneri,the inflammation is more severe, as with the watery diarrhea turns bloody and
may progress to dysentery, with its characteristic small-volume bloody, mucoid stool passed
many (10 to >40) times per day with abdominal cramps, and tenesmus.
-The most severe infections due to S. dysenteriae type 1.
o Treatement
-Because of the mild nature of S. sonnei infection in well nourished no treatment is required.
-In the case of bloody diarrhea or dysentery, antibiotics are the mainstay of treatment. -
empirical therapy of adults with bloody diarrhea or dysentery can be initiated with
ciprofloxacin. A reliable oral alternative is azithromycin.
o complications of Shigella : bacteremia, metabolic disturbances →hypovolemia,
hyponatremia, protein-losing enteropathy, leukemoid reaction, neurologic disease
,reactive arthritis, S. dysenteriae 1 cause hemolytic uremic syndrome.
 GENUS: BRUCELLA
o Genus Features
-Gram-negative rods, aerobic
-Zoonosis
-Facultative(in our lectures it is obligatory) intracellular pathogen.
-Obligate aerobes, grow on blood agar and enriched media (trypticase-soy).
-Brucella utilize CHO with no acid or gas, reduce nitrate, catalase , oxidase & urease positive
and H2 S is produced by many strains.
-killed by milk pasteurization for 10 min at 60oC
-B.melitensis (goats & sheep). -B.abortus (cattle). -B.suis(pigs). -B.canis(dogs)
o Antigenic structure: -The 2 lipopolysaccharide antigens A&M are present in different
proportions in the 4 spp. -Superficial L Ag also present that resembles the Vi Ag of
Salmonellae.
o Pathogenesis:
-Facultative intracellular parasite (localizes in cells of the RES, reticuloendothelial
system) → septicemia→many killed by macrophages, but some survive within the cells
protected from Abs.
-Granulomatous response with central necrosis→ can progress to focal abscesses.
-Endotoxin
o Community
Mode of transmission 1. Contact through breaks in the skin with animal tissues, blood,
urine, vaginal discharges, aborted fetuses and especially placentas 2. ingestion of raw milk
and dairy products (unpasteurized cheese) from infected animals. 3. Airborne infection
occurs in pens and stables for animals, and for humans in laboratories and abattoirs.
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o Medicine
*B.abortus →mild disease without suppurative complications and non caseating granuloma.
*B.canis →mild disease. *B.suis →chronic disease with suppurative and caseating
granulomas. *B.melitensis → more acute and severe disease.
 CLINICAL MANIFESTATIONS • High swinging undulating temperature (hence named

Undulant Fever) • Rigors • Lethargy • Headache • Joint and muscle pains • Scrotal
pain.
Presentations often fit into 1 of 3 patterns : • Febrile illness that resembles typhoid, but is
less severe. • Fever and acute monarticular arthritis (typically of the hip or knee) in a young
child. •Long-lasting fever, depression, and low back or hip pain in an older person.
 Physical signs: - General : Non-specific, e.g. enlarged lymph nodes and spleen.
 Local manifestations
-SKELETAL •Arthritis •Osteomyelitis •Spinal spondylitis •Paravertebral or psoas abscess.
-NEUROLOGICAL • Neurobrucellosis →usually as meningitis.
-Others :Genitourinary disease, especially epididymo-orchitis. •Endocarditis — 1 percent.
• Hepatic abscess.
 DIAGNOSIS : Non-specific Lab Tests • CBC→WBC are usually normal to low;

pancytopenia (low WBC, RBC and platelets) can occur • XR of spine and
echocardiography may be helpful evaluating focal disease but do not provide a
definitive diagnosis. •CSF test in neurobrucellosis may show elevated WBC and
protein.
• Definitive diagnosis depends on the isolation of the organism
 Specific tests
1-culture : of blood , bone marrow (high yield), synovial fluid or CSF (low yield).
Lets go back to micro!..... culture on Trypticase – soy broth and sub culture every 3-5 days on
solid media (under aerobic and 10% CO2 ), keep blood for 4wks before being discard as
negative. Biochemically they are (oxidase positive & urease positive). The isolated brucellae
typed by H2 S production and agglutination by specific antisera.
2- serology: a-Agglutination test (Rose Bengal) For detection of IgG Ab. IgG titers >1:80
indicate active infection. Detect 95% of acute infections.
This test can give: false positive because of cross reaction with other infection.
What to do? → application of 2- Mercaptoethanol test. the addition of 2me will destroy IgM
and leaves IgG..
False negative because of the presence of blocking Abs (IgA) which appear during subacute
stage and remain for years causing a negative test in low serum dilution.
What to do now?→ increase dilution or using coombs antiglobulin method(patient serum +
Brucella antigen +Anti human globulin).
b-ELISA.
3- biopsy: Biopsied samples (e.g., lymph node, liver) may show noncaseating granulomas
with absence of Acid Fast Bacilli.
 TREATMENT :
Adults with non-localised disease: Doxycycline + gentamicin IV or Doxycycline + rifampicin.
Neurobrucellosis : Doxycycline + rifampicin + ceftriaxone until CSF is clear.
Endocarditis : Almost always needs surgical intervention and antibiotics.
Pregnancy : Rifampicin + co-trimoxazole.
Caution!! in last week of pregnancy due to displacement of bilirubin from albumin by drugs
(co-trimoxazole) and risk of kernicterus to the fetus.
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Surgery indications: • Endocarditis • Drainage or excision of abscesses, • Spinal epidural
abscess.
Note: Brucella spp. survive for long periods within the reticulo-endothelial
system→chronicity and relapse so patient needs follow up.
 GENUS: VIBRIO
o Genus Features
-Gram-negative curved rod with polar flagella
-Oxidase positive
-Growth on alkaline, but not acidic, media (TCBS, thiosulfate citrate bile salt sucrose
medium).
*Vibrio cholera * Vibrio parahaemolyticus *Vibrio vulnificus
Vibrio cholerae
-“Shooting star” motility inactivated by specific serum
-ferment glucose, sucrose & mannose but not lactose.
-V.cholera killed by acidity and destroyed by 55C for 15min.
-It reduce nitrates -nitrite with production of Indole
o Antigenic structure of V.cholera
-Based upon The O, lipopolysaccharide, antigen , there are 139O.
-The causative agent of almost all cholera cases is O1. This can be classified into classic and
ELtor according to biochemical reactions (biologically) , and can be classified serologically
into Inaba, Ogawa and the very rare Hikojima.
-O139 also cause classical cholera, and this strain shares the other non- O1 cholera strains
the presence of a polysaccharide capsule .
-Vibrio which lack O Ag called non agglutinable vibrio which cause cholera like disease.
o Transmission
-Fecal-oral spread; sensitive to stomach acid
-Requires high dose (>107 organisms), if stomach acid is normal
o pathogenesis
The microorganism adhere to epithelial cells of brush border of the gut, multiply and secrete
-mucinase enzyme which dissolves the protective glycoprotein coating the intestinal cells.
-Cholera enterotoxin (choleragen) composed of 2 subunits (A&B), B unit is binding
facilitating toxin entry, activation of A subunit → increase level of intracellular CAMP
Prolong hypersecretion of water&electrolyte causing watery diarrhea without
inflammatory cells (non– invasive).
o Medicine
Cholera Clinical Presentation:
symptoms begin with the sudden onset of painless watery diarrhea that may quickly become
voluminous and is often followed by vomiting, abdominal cramps, probably from distention
of loops of small bowel, Fever is typically absent.
Diarrhea in cholera : Profuse watery diarrhea is a hallmark of cholera, Stool volume during
cholera is more than that of any other infectious diarrhea, The characteristic cholera stool is
an opaque white liquid that is not malodorous and often is described as having a rice water‖
appearance. Dehydration can develop with remarkable rapidity, within hours after the onset
of symptoms.
Metabolic Panel in cholera:sodium , Hyperglycemia, potassium is normal in the acute
phase but hypokalemia with disease progression, elevated anion gap metabolic acidosis
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result from increase in serum lactate, protein, and phosphate levels., Patients have elevated
blood urea nitrogen and creatinine levels, Calcium and magnesium levels are usually high as
a result of hemoconcentration.
Diagnosis : mainly clinical especially in outbreaks. In laboratory confirmation follow the

following steps :
1-Microscopical examination: gram neg. curved rods
2-Motility test: observing cholera motility by two techniques a-by stabbing the micro-
organism with needle into semisolid media, b-Hanging drop preparation(watch them in
youtube if you like).
3-Cholera immobilization test: treating cholera with specific antisera make them immobile.
4-culture : ( T . C . B . S .) alkaline media→ yellow colonies.
5-Biochmical tests
*Cholera red test: It reduce nitrates -nitrite with production of Indole
*Oxidase test: oxidase +
6-Typing of the isolated micro-organism with specific antisera.
o Treatement
The mainstay of treatment for cholera is the correction of hypovolemic dehydration.
Rehydration is accomplished in 2 phases: rehydration and maintenance. The degree of
dehydration will determine the route, rate, and type of fluid used for volume replacement.
Oral rehydration solutions is used for mild disease. Intravenous volume repletion indicated
in Patients who have lost more than 10 percent of body weight from dehydration or who
are unable to drink because of vomiting or mental status changes. Lactated Ringer solution is
preferred over isotonic sodium chloride solution because saline does not correct metabolic
acidosis. Dextrose-containing solutions should not be used for volume repletion.
Antimicrobial therapy for cholera is an adjunct to fluid therapy and is not an essential
therapeutic component. If antimicrobial therapy is to be initiated, it should be given when
the patient is first seen and cholera is suspected. The use of quinolones is contraindicated in
children with cholera.
Vaccine : The cholera vaccine Vaxchora is a live, weakened vaccine administered as a single,
oral liquid dose at least 10 days before travel to a cholera affected region.
Test yourself part-4-

Case scenario for questions 1-4
While you are caring for villagers stricken with cholera, you encounter a 22-year-old truck
driver. He has the typical rice-water stools and has had seven bowel movements today
before noon. He is thirsty but is able to hold a coherent conversation with you and can stand
up without feeling light-headed. His HR is 87 bpm, and BP is 105/70 mmHg.
1)Which of the following correctly describes the causal agent?
(A) Gram-negative curved rod; toxin that increases cAMP
(B) Gram-negative curved rod; toxin that inhibits protein synthesis
(C) Gram-negative rod; toxin that increases cAMP
(D) Gram-negative rod; toxin that inhibits protein synthesis
(E) Intoxication with a heat labile toxin that blocks the release of acetylcholine
2)All of the following is true regarding the causative agent except :

a-nitrate reducer b-oxidase positive c-lactose fermenter. d-requires alkaline media.
3)Which of the following statements regarding vibriosis is false?

A. Achlorhydia increases susceptibility to cholera
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B. hypokalemia and metabolic acidosis are possible consequences.
C. the vaccine is a live attenuated vaccine.
D. Fever often precedes the onset of diarrhea in cholera.
E. The stool in cholera diarrhea usually contains flecks of mucus.
4) What is the most appropriate treatment for our patient?

A. Erythromycin 250 mg orally four times daily for 3 days
B. IV fuid replacement with normal saline 100 mL/kg over 3 hours
C. IV fuid replacement with lactated Ringer’s solution 100 mg/kg over 3 hours
D. Mix 0.5 teaspoon of table salt and 6 teaspoons of table sugar with 1 L of sterile water and
have the patient drink up to 2 L of this solution daily
E. No treatment is necessary

A 45-year-old woman presents to the emergency department with intense pain in her lower
back and a burning sensation upon urination. A urine culture was taken and plated on
MacConkey agar. Gram-negative rods that did not ferment lactose were identified.
5)virulence factor of the causal agent is most important to pathogenesis?

(A) Capsule(B) Catalase(C) Coagulase(D) Exotoxin(E) Urease
6)Which of the following is a likely complication due to infection with the causal agent?
(A) Diarrhea(B) Kidney stones(C) Pseudomembranous colitis(D) Stomach cancer(E) Vomiting

Mr. Hou is a 56-year-old former pig farmer from China who has been in the United States for
the past year visiting his sister. Shortly after arriving, he began experiencing fevers.
Curiously, he has noted that while the fever has persisted for a year, it has followed the
unusual undulating pattern. The fever would usually last for 2 weeks and then relent for
about 2 weeks at a time before returning. He also experienced joint pains and myalgias
during his times of fever. More recently, he has experienced lower back pain with
movement and at rest. He denies any weakness or numbness. A serologic investigation
returns positive for immunoglobulin (Ig) G antibodies for Brucella.
7)Which is true regarding the causative agent :
a-anaerobic gram negative rod.
b-resistant to heating.
c-produce exotoxin important in pathogenesis.
d-grows slowly in culture media.
e-an enterobacteriaccae member .
8)Which of the following statements regarding his condition is true?
A. A safe and effective human vaccine is available for brucellosis.
B. In this patient, Brucella melitensis is more likely than Brucella suis.
C. Prior to starting treatment, coinfection with tuberculosis should be excluded.
D. The presence of IgG antibodies is nonspecifc. Given the atypical presentation, this likely is
not a true Brucella infection
E. Mr.Hou is suffering from acute brucellosis.
9)What is the appropriate treatment ?
a-ampicillin+gentamicin b-doxycycline+rifampicin
c-cefriaxone+ciprofloxacin d-azithromycin+chloramaphenicol.
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Five healthy college roommates develop rapid onset of abdominal pain, cramping, fever to
38.5°C, vomiting, and copious non bloody diarrhea while camping. They immediately return
for hydration and diagnosis. A stool culture grows Salmonella enteritidis.
10) all of the following statements regarding their clinical syndrome are true except:
A. sometimes present with bloody diarrhea.
B. Bacteremia occurs in less than 10% of cases.
C. The most likely source was undercooked eggs.
D. There is no vaccine available for this illness.
E. They have enteric fever.
A 68-year-old woman on chemotherapy for leukemia has developed sepsis due to an
infection with Escherichia coli. The following day the patient develops septic shock and dies.
11)The structure on the bacterium most likely responsible for causing septic shock in this
patient is
(A) capsule (B) lipopolysaccharide (C) pili (D) spore (E) teichoic acid
A 35-year-old man who is positive for HIV develops sepsis with the subsequent development
of a necrotic lesion on the buttock that has a black center and an erythematous margin.
12)Which of the following is the most likely causal agent?
(A) Bacillus anthracis
(B) Clostridium perfringens
(C) Enterococcus faecalis
(D) Pseudomonas aeruginosa
(E) Staphylococcus aureus
Case scenario for question 13-14-15
You are caring for a previously healthy 65-year-old man who was admitted to the hospital
yesterday after having fevers for a week at home. On admission, his temperature was
39.7°C, HR was 68 bpm, and BP was 110/60 mmHg. Examination of his skin reveals a faint,
salmon-colored, blanching, maculopapular rash located primarily on the trunk and chest. He
complains of moderate abdominal pain and nausea. While blood culture reveals no
organisms, bone marrow culture grows gram-negative rods. The bacteria produce acid on
glucose fermentation, reduce nitrates, and do not produce cytochrome oxidase or ferment
lactose. Closer inspection shows that they are motile by means of flagella.
13)What other characteristic the causative agent has?
a-increasing motility with heating.
b-survive freezing in water for long periods.
c-requires small infecting dose.
d-widespread among animal reservoirs.
14)On his second week of illness he is likely to show all of the following except:
a-cough b-hepatosplenomegaly c-constipation d-delirium e-GIT hemorrhage
15)regarding the diagnosis of this patient illness :
a-stool cultures are positive if performed.
b- widal test is the gold standard in the diagnosis.
c- most likely to show rising serum Anti-O titer that is persistent for years.
d-after the second week urine cultures may be positive.
e-positive Anti-Vi is a marker of disease relapse.
Case scenario for question 16-17
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A 36-year-old woman develops severe crampy abdominal pain, fever to 40°C, nausea, and
malaise. The next day, she begins having bloody mucopurulent diarrhea with worsening
abdominal pain and continued fever.A stool examination shows many neutrophils, and
culture grows Shigella fexneri.
16)Regarding the causative agent :
a-motile gram negative rod
b-K antigen used in serotyping
c- produces H2S
d- cannot grow on simple media
e-most common cause of shigella
17)Which of the following statements regarding her clinical syndrome is true?
A. An effective vaccine for travelers is available.
B. Antibiotic therapy prolongs the carrier state and should not be administered unless she
develops bacteremia.
C. Antimotility agents are effective in reducing the risk of dehydration.
D. Ciprofoxacin is recommended therapy.
E. pathogenesis is mainly by toxin production causing enterocyte death.
Case scenario for question 18-19
A 27-year-old woman, after returning home from her honeymoon presents to your acute
care clinic with a complaint of burning urination for the past 4 days. Yesterday, she noticed
that her left flank and her back were also painful, and she began having fevers up to 102°F.
Her examination is notable for temperature of 39°C, HR of 105 bpm, and BP of 105/65
mmHg, left costophrenic angle tenderness, and an otherwise benign abdominal/pelvic
examination. Clean catch urinalysis shows positive leukocyte esterase, a high WBC count,
and no epithelial cells. You suspect pyelonephritis.
18) Which of the following organisms is the most common cause of this infection?
(A) A gram-negative diplococcus, which is oxidase positive but does not ferment
maltose
(B) A gram-positive coccus, which is catalase positive and coagulase negative
(C) An optochin-resistant, catalase-negative, gram-positive coccus
(D) A gram-positive bacillus grown on a low oxidation-reduction medium
(E) A gram-negative bacterium capable of reducing nitrates to nitrites
19)Cystitis is associated with all of the following EXCEPT:
A.Urgency
B.pain while urinating
C.Fever
D.Absence of renal scarring
E.Sexual activity in females
20) All of the following statements regarding intestinal disease caused by strains of Shiga
toxin– producing enterohemorrhagic E coli are true EXCEPT:
A. Antibiotic therapy lessens the risk of developing hemolytic-uremic syndrome.
B. Ground beef is the most common source of contamination.
C. Gross bloody diarrhea without fever is the most common clinical manifestation.
D. no pus cells are found in stool examination.
E. O157:H7 is the most common serotype
21)Hemolytic-uremic syndrome is typically a complication of infection with E. coli O157:H7
or other Shiga toxin–producing strain of E. coli. The same process, microangiopathic
hemolytic anemia with renal failure, can also follow infection with:
A.Salmonella typhi or Campylobacter jejuni
B.Shigella fIexneri
C.Shigella sonnei
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D.Shigella dysenteriae serotype 1
E.Any species or serotype of Shigella
.
 GENUS: TREPONEMA
o Genus Features
-Spirochetes: spiral with axial filament (endoflagellum)
-Poorly visible on Gram stain but gram-negative envelope
o Species of Medical Importance—Treponema pallidum
1-Treponema pallidum
-Thin spirochete, not reliably seen on Gram stain
-Basically a gram-negative cell envelope
-Outer membrane has endotoxin-like lipids.
-Axial filaments = endoflagella = periplasmic flagella
-Cannot culture in clinical lab; serodiagnosis
-easily killed by drying or heating at 42C for an hr
-Is an obligate pathogen (but not intracellular)
o Community
-Concurrent HIV infection may increase the risk of CNS syphilis.
-Mode of transmission: 1- Direct contact with infectious exudates during sexual contact
2-Trans placental infection of the fetus occurs during the pregnancy of an infected woman.
3-Transmission can occur through blood transfusion if the donor is in the early stages of
disease.
- Syphilis is contagious during its primary and secondary stages, and sometimes in the early
latent period.
o Medicine
 Presentation :
1-primary syphilis: The disease starts as a painless sore(chancre) typically on genitals, rectum
or mouth about three weeks after exposure. it may be hidden within the vagina or rectum,
The chancre will heal on its own within six weeks. A firm, non fluctuant, painless satellite
lymph node (bubo) commonly follows.
2-Secondary syphilis: Rash that begins on trunk but eventually covers entire body even the
palms of hands and the soles of feet. This rash is usually not itchy and may be accompanied
by wart-like sores in the mouth or genital area(condyloma lata), with associated
lymphadenopathy & mild constitutional Symptoms. These signs and symptoms may
disappear within a few weeks or repeatedly come and go for as long as a year.
Latent syphilis: If untreated, the disease moves from the secondary to the latent (hidden)
stage, No symptoms. Signs and symptoms may never return or pass into tertiary syphilis (in
1\3 of patients).
3-Tertiary (late) syphilis: many years after the initial infection (unless the patient has HIV
→fast progression), The disease may damage brain, nerves, eyes, heart, blood vessels, liver,
bones and joints.
o Complications :
• Small bumps or tumors : as gummas.
• Neurological problems :as Stroke,Meningitis,Deafness,Visual problems,Dementia
• Cardiovascular problems : These may include bulging (aneurysm) and inflammation of the
aorta, Syphilis may also damage heart valves.
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• HIV infection
o Pediatrics
Congenital Syphilis:
-Approximately 30% to 40% of fetuses are stillborn
- Approximately 75% of live born infants are asymptomatic at birth
-Symptoms develop between 3rd and 14th weeks after birth.
Clinical symptoms split into early or late (2 years is cutoff)
Congenital Syphilis: Key Features • Skeletal abnormalities (osteochondritis & periostitis)
• Pseudoparalysis • Persistent rhinitis(snuffles) • Maculopapular/vesicular rash (particularly
on palms and soles or in diaper area)
o Diagnosis :
Syphilis can be diagnosed by testing samples of: • Blood (serodiagnosis)
• Fluid from sores(for the spirochete detection useful in early syphilis)
Fluid from sores can be tested using Dark-Field Examination or Immunofluorescence
• Cerebral spinal fluid: for nervous system complications of syphilis..
Nontreponemal tests: Test for reagin Ab using cardiolipin (from beef heart)Ag, used as
screening tests for syphilis,they include 1. VDRL (Venereal Disease Research Laboratory) test
2. RPR (Rapid Plasma Reagin) test.
These tests are non specific tests and false positive reactions are seen in Influenza, carditis
and connective tissue diseases.
Treponemal antibody tests: Measure Ab against T pallidum antigens(specific). The tests are
confirmatory for positive result from a nontreponemal test. They include 1. T pallidum
hemagglutination (TPHA) 2. T pallidum immobilization (TPI) test 3. Treponemal antibody
tests using the EIA for T pallidum 4. Fluorescent treponemal antibody absorbed (FTA-ABS)
test.
o Treatment: The preferred treatment at all stages is penicillin. In its early stages ,
syphilis can be cured by a single injection .Penicillin is the only recommended
treatment for pregnant women with syphilis. Women who are allergic to penicillin
can undergo a desensitization process that may allow them to take penicillin.
Once cured, syphilis doesn't recur.
o Bordetella pertussis
-Small gram-negative, aerobic rods
-Encapsulated organism
o Transmission—respiratory droplets
-Pertussis is extremely contagious, with attack rates as high as 100% in susceptible
individuals exposed to aerosol droplets at close range. Neither natural disease nor
vaccination provides complete or lifelong immunity against pertussis re-infection(subclinical)
or disease.
o Clinical manifestations:
1- The catarrhal stage (~ 2 wk): non distinctive symptoms of congestion and rhinorrhea with
low-grade fever, patients usually are highly contagious in this stage.
2- The paroxysmal stage (~ 4 wk): the cough begins as a dry, intermittent, irritative hack and
evolves into the inexorable paroxysms that are the hallmark of pertussis. During the episode
of coughing, well-appearing toddler suddenly expresses a machine-gun burst of
uninterrupted cough on a single exhalation. When coughing ceases and a loud whoop
follows. Post-tussive emesis is common, and exhaustion is universal., patients usually are
non contagious in this stage.
3- The convalescent stage ( ~ 2 wk): the number, severity, and duration of episodes
diminish.
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o Exceptions from typical manifestations :
1-The infant may develop chocking, cyanosis and sometimes apnea during the episodes.
2- Adolescents(>10yrs.) and previously immunized children have foreshortening of all stages
of pertussis.
o Diagnosis: mainly clinical. Isolation of B. pertussis in culture remains the gold
standard for diagnosis. Leukocytosis (15,000-100,000 cells/mm3) due to lymphocytosis is
characteristic in the catarrhal stage. Chest radiographic findings are not diagnostic.
o Treatement :
-Goals of therapy are to limit the number of paroxysms, and to maximize nutrition, rest, and
recovery without sequelae.
-Antimicrobials given early(in catarrhal stage) may moderate symptoms, but they are of little
benefit in the paroxysmal stage except to limit spread of organisms.
-Macrolides are preferred agents(azithromycin or erythromycin.
-Isolation : Patients with suspected pertussis are placed in respiratory isolation with use of
masks by all health care personnel entering the room. A macrolide agent should be given
promptly to all household and other close contacts, regardless of age, history of
immunization, and symptoms.
o Complications:
1-Pneumonia due to the Pertussis organism or, more frequently, to secondary bacterial
invasion is a common complication.
2-Infants <6 mo of age have excessive mortality and morbidity→apnea.
3-Increased intrathoracic pressure during coughing can result in conjunctival and sclera
hemorrhages, epistaxis, hemorrhage in the CNS, pneumothorax and subcutaneous
emphysema,and umbilical and inguinal hernias.
Note: Protective antibody to pertussis does not cross the placenta. This means that the
newborn is completely vulnerable to infection →should receive vaccine
o Chlamydia
o Micro
-Obligate intracellular bacterium; cannot make ATP
-Found in cells as metabolically active, replicating reticulate bodies
-Infective form: inactive, extracellular elementary body
-Not seen on Gram stain; atypical peptidoglycan layer →lacks muramic acid.
-C.trachomatic has at least 15, C.psittaci and C.pneumoniae each have 1 immunotype
Transmission:
-C.trachomatis :sexual contact and at birth; trachoma is transmitted by hand-to-eye
contact and flies
-C.pneumoniae : from humans by resp. aerosols.
-C.psittaci : from birds by inhalation of bird dry feces.
o Medicine :
-Chlamydia is known as a ‘silent’ infection because most infected people are asymptomatic
and lack abnormal physical examination findings.
-Types of Chlamydia trachomatis infection: • Eye (Trachoma) • Genital organs
• Lymphogranuloma venereum.
 Trachoma:
is a chronic keratoconjunctivitis and is the most common cause of avoidable blindness. In
endemic areas, the disease is most common in children.
Symptoms : The onset is usually insidious. Early symptoms include conjunctival irritation
and blepharospasm. The early follicles are characteristic. Scarring causes inversion of the
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lids so that the lashes rub against the cornea. The cornea becomes vascularized and
opaque. The problem may not be detected until vision begins to fail.
Diagnosis: 1- Conjunctival scrapings for staining with iodine or immunofluorescence→
Cytoplasmic inclusion
2- Chlamydia may be isolated with culture.
Rx: A single dose of azithromycin.
 Chlamydial infection in men:
-presents in a similar way to gonorrhoea; however, urethral symptoms are usually milder
and may be absent in over 50% of cases. Conjunctivitis is also milder than in gonorrhoea;
pharyngitis does not occur.
- Without treatment, symptoms may resolve but the patient remains infectious for several
months.
 Chlamydial infection in women:
- The cervix and urethra are commonly involved , Infection is asymptomatic in about 80% of
patients but may cause vaginal discharge, dysuria and intermenstrual and/or postcoital
bleeding
- Some infections may clear spontaneously but others persist, Untreated chlamydia may
increase a person’s chances of acquiring or transmitting HIV for both male and female.
- PID, with the risk of tubal damage and subsequent infertility or ectopic pregnancy, is a rare
but important long-term complication. Lower abdominal pain and dyspareunia are features
of PID. Perinatal transmission may lead to ophthalmia neonatorum and/or pneumonia in the
neonate.
 Chlamydia pneumonia:
a- type of atypical bacterial pneumonia characterized by a- long incubation periods (3 to 4
weeks) b- wide spectrum of clinical symptoms c- Has a higher incidence in elderly adults.
C. pneumoniae presented with • Laryngitis • Pharyngitis • Coryza • Malaise • Fever • Cough
• Headache
Extrapulmonary manifestations including: • Meningoencephalitis • Guillain-Barré syndrome
• Reactive arthritis • Myocarditis.
-Since the diagnosis of C. pneumoniae is often not established, treatment commonly begins
with empiric therapy for atypical pneumonia.
 Chlamydophila psittaci:
-The symptoms of the disease range from inapparent illness to systemic illness with severe
pneumonia, It presents chiefly as an atypical pneumonia.
-In the first week of psittacosis: the symptoms mimic typhoid fever: prostrating high fevers,
joint pains, diarrhea, conjunctivitis, nose bleeds and low level of white blood cells in the
blood.
-The second week: acute bacteremic pneumococcal pneumonia with continuous high fevers,
cough and dyspnea. X-rays show patchy infiltrates or a diffuse whiteout of lung fields.
 Chlamydia Dx: 1- cell culture 2- Chlamydial antigens can be detected by ELISA

3- Organisms can be identified in exudates by fluorescent antibody staining, ELISA, or by use
of DNA probe (hybridyzation).4- Cytoplasmic inclusion seen with Giemsa's stain or by
immunofluorescence.5- Serologic tests reliable in diagnosis of chlamydial infection but not
for C.trachomatis.
 RX: 1- single dose of azithromycin or 2-doxycycline for 7 days.

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A 22-year-old college student presents for the evaluation of a painless non pruritic rash of 1
week in duration. Three months ago, he engaged in unprotected sexual intercourse. Two
months ago, he noted a penile papule that evolved to a painless, clean-based, and indurated
ulcer. He did not seek medical attention because the ulcer healed spontaneously.
Subsequently, he developed the rash. He complains of no other symptoms and has no
stigmata of ocular or neurologic involvement. He does not have HIV.
1)Regarding the condition of this patient :
a- if untreated , neurologic complications will manifest in one month.
b-culture of the lesions will reveal the agent and confirms the diagnosis.
c-cannot be acquired through transfusion.
d-the condition is in its primary stage.
e-non-specific serological tests are the first step in diagnosis.
2)False positive non-treponemal tests can occur in :
a-EBV infection
b-SLE
c-influenza
d-b&c
e-non of the above
3)What is the most appropriate antibiotic regimen?
A. Azithromycin 1000 mg orally for one dose
B. Benzathine penicillin G 2.4 mU IM for one dose
C. Doxycycline 100 mg orally twice a day for 14 days
D. Doxycycline 200 mg orally for one dose
E. Penicillin G 18–24 mU/d IV for 14 days
A 6 years old child is brought by his parents to the clinic. Approximately two weeks ago, he
developed an upper respiratory syndrome with low grade fever, coryza, some cough, and
malaise. The fever and coryza have improved but over the last 4 days he has an episodic
cough that is often severe enough to result in vomiting. He is afebrile, and while not
coughing, his chest examination is normal. During a coughing episode, there is an occasional
inspiratory whoop. Chest radiograph is unremarkable.
4)Which of the following is true regarding his likely illness?
A. A fuoroquinolone is recommended therapy.
B. antibiotics ,if given ,will only affect communicability.
C. diagnosis is routinely done by cultures.
D.primary Pneumonia is usually more common than secondary pneumonia as a
complication.
E. reassure his parents that his illness will not last more than few days.
A 20-year-old woman is 36 weeks pregnant and presents for her first evaluation. She is
diagnosed with C trachomatis infection of the cervix.
5)Which of the following statements regarding Chlamydia trachomatis infection is false?
A.Up to 75% of women infected with C. trachomatis have no symptoms of disease
B.Approximately 50% of males infected with gonorrhea are co-infected with C. trachomatis
C.serology is the gold standard in diagnosis.
D.Uncomplicated genital infection in men and non pregnant women can be treated with a
single dose of azithromycin.
6)Upon delivery, what complication is her infant most at risk for?

A. Jaundice B. Hydrocephalus C. Hutchinson triad D. Conjunctivitis E. Sensorineural deafness
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Prepared by :
Haitham nabeel
 GENUS: MYCOBACTERIUM
o Micro
Genus Features
 Acid fast rods with a waxy cell wall l Obligate aerobe
 Cell wall
− Unique: high concentration of lipids containing long chain fatty acids called mycolic acids.
− Wall makes mycobacteria highly resistant to:
º drying º Many chemicals (including acids and bases).
 Sensitive to UV
 Mycobacterium tuberculosis
-Auramine-rhodamine staining bacilli -Acid fast
-Aerobic, slow growing on Lowenstein-Jensen medium
o Pathogenesis
 Facultative intracellular organism→ grows within macrophages (most important)
 Sulfatides (sulfolipids in cell envelope)
-Inhibit phagosome-lysosome fusion, allowing intracellular survival
 Cord factor
− Causes serpentine growth in vitro − Inhibits leukocyte migration
 Tuberculin (surface protein) along with mycolic acid → delayed hypersensitivity and cell-
mediated immunity (CMI)
 Granulomas and caseation mediated by CMI
 No exotoxins or endotoxin; damage done by immune system.
o Now let's follow TB bacilli in their journey inside the body!

After being inhaled, mycobacteria reach the alveoli, multiply in the pulmonary epithelium or
macrophages. This initial phase occurs in a small bronchiole or alveolus in the base . their
presence initiates an inflammatory reaction, the bacteria proliferate and are carried by
lymphatic drainage to the lymph nodes and beyond to set up additional foci. the place
where mycobacteria infection sets is called ghon focus , and with the draining lymph nodes
it is named ghon complex. This initial phase of the infection is usually mild or asymptomatic
and results in exudative lesions in which fluid and polymorphonuclear leukocytes
accumulate around the bacilli.
Tubercle formation: It consists of a central area of large, multinucleated giant cells
containing tubercle bacilli, a midzone of pale epithelioid cells, and a peripheral collar of
fibroblasts and mononuclear cells. Tissue damage is produced by the destruction of both
bacilli and phagocytes. The center of the tubercle develops caseous (cheesy) necrosis. The
initial phase + tubercle formation = primary tuberculosis.
Primary tuberculosis follows one of two courses: -1-If the lesion arrests, the tubercle
undergoes fibrosis and calcification, although viable but non proliferating organisms may
persist. this happens in most of the time .
2-If the lesion breaks down, the caseous material is discharged, and a cavity is created that
can facilitate spread of the infection. The organisms are dispersed by the lymph and the
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bloodstream and can seed the lungs; regional lymph nodes; or various distant tissues, such
as liver, spleen, kidneys, bone, or meninges, known as miliary (disseminated) tuberculosis.
Secondary disease–reactivation:
Occurs later in life under conditions of reduced T-cell immunity. It is caused by dormant
bacilli in a primary lesion especially ones with high oxygen tension (lung apices,renal) .
Destruction of the lung tissue leads to air-filled cavities where the bacteria replicate actively.
Bacterial populations in such lesions often become quite large, and many organisms are
shed (for example, in sputum).
o Community
Facts:
1-10% of those initially infected will eventually develop active disease, half of them during
the first 2 years following infection. 90% of untreated infected individuals will never develop
active TB.
2-In infants the disease is often disseminated (miliary) or meningeal.
3-Extra pulmonary TB occurs less commonly (30%) than pulmonary TB (70%).
It may affect any organ, in order of frequency: lymph nodes, pleura, pericardium…etc.
4-A smear positive for acid-fast bacilli (AFB) is indicative of high infectiousness. 65% of
patients with sputum smear-positive pulmonary tuberculosis, if untreated will die within 5
years, most of them within 2 years.
o Tuberculin skin test :
A measured amount of PPD is injected intradermally in the forearm.
• It is read 48 to 72 hours later for the presence and size of an area of induration(hardening)
at the site of injection.
•used to document contact with the tubercle bacillus, they do not confirm that the patient
currently has active disease.
•Among persons with active TB disease 10%–20% may have no reaction to PPD(purified
protein derivative) a negative skin test does not therefore rule out active TB disease.
•An induration of tuberculin skin test of 5 mm or more is considered positive among • HIV-
infected persons • Persons on immunosuppressive treatment • Persons showing fibrotic
lesions on chest X-rays • Recent close contacts of infectious TB patients.
•A diameter of 10 mm or more is considered positive among persons with high-risk
conditions (e.g. diabetes mellitus, hematological disorders, injection drug use, end-stage
renal disease, rapid weight loss).
•Any reaction of 15 mm or more should be considered positive among low-risk persons.
•The skin test may boost to react to tuberculin and cause a positive reaction in subsequent
tests. Boosting also reported in persons who have received BCG. A 2-step testing procedure
1–3 weeks apart will distinguish boosted reactions and reactions due to new infection.
should be done to people who will be retested periodically (e.g. health care workers).
5-TB mortality and morbidity rates increase with age, and higher in males than in females,
morbidity is highest among working-age adults.
Mode of transmission: Exposure to tubercle bacilli in airborne droplet nuclei. Health care
workers are exposed during procedures such as bronchoscopy or intubation and at autopsy.
Extrapulmonary tuberculosis (other than laryngeal which is highly contagious) is generally
not communicable.
Period of communicability: Theoretically, as long as viable tubercle bacilli are discharged in
the sputum. The degree of communicability depends on: • Number of bacilli discharged
• Virulence of the bacilli • Adequacy of ventilation • Exposure of bacilli to sun or UV light.
Children with primary tuberculosis are generally not infectious.
Effective antimicrobial chemotherapy usually eliminates communicability within 2–4 weeks.
The risk of developing disease is highest in children under 3, lowest in later childhood, and
high again among young adults, the very old and the immunosuppressed.
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Important points in preventive measures :
Directly Observed Treatment Supervised (DOTS strategy) should be used when possible and
can be administered twice weekly. Not more than 1 month’s supply of medication should be
given at any one time.
BCG immunization: alive attenuated vaccine(attenuated M. bovis.) is considered for persons
from areas of high tuberculosis prevalence. BCG immunization protect against TB meningitis
and disseminated disease in children under 5 . Protection from BCG vaccine may persist for
as long as 20 years in high incidence situations, others have shown no protection at all.
administration route is intradermal.
Treating latent TB : indicated for 1-Persons with HIV infection and a positive PPD who do not
have active TB disease should receive treatment for latent TB infection.
2-usually recommended for persons who are in contact with TB infection and in whom TB
disease has been ruled out.
It consists of isoniazid for 6–12 months.
o Pediatrics
Interferon-γ Release Assays (IGRA): Blood tests detect IFN- γ generation by the patient’s T
cells in response to specific M. tuberculosis antigen. Its advantages include the need for only
one patient encounter, lack of cross reaction with BCG vaccination and most mycobacteria,
and absence of boosting (increasing reaction to the TST with serial testing). In persons who
received a BCG vaccination, the IFN- γ release assays are the preferred test.
CLINICAL MANIFESTATIONS AND DIAGNOSIS:
 Primary Pulmonary Disease:
Presentation: Nonproductive cough and mild dyspnea are the most common symptom,
Systemic complaints such as fever, night sweats, anorexia, and decreased activity occur less
often while some infants develop failure-to-thrive. These pulmonary symptoms and signs
are occasionally alleviated by antibiotics, suggesting bacterial superinfection.
Diagnosis: isolation of M. tuberculosis through sputum specimens for culture.
 Pleural Effusion:
Presentation: clinically significant effusions occur months to years after the primary
infection. They are usually unilateral but can be bilateral. Clinical onset is often sudden,
characterized by low to high fever, shortness of breath, chest pain on deep inspiration, and
diminished breath sound.
Diagnosis: Examination of pleural fluid and the pleural membrane biopsy is important to
establish the diagnosis of tuberculous pleurisy.
 Pericardial Disease:
Presentation: The presenting symptoms are nonspecific, including low-grade fever, malaise,
and weight loss. Chest pain is unusual in children. A pericardial friction rub or distant heart
sounds.
Diagnosis: Pericardial fluid exam for stain, and culture is diagnostic.
 Lymphohematogenous (Disseminated) Disease:
Presentation: Lymphohematogenous spread occurs in every TB infection and is usually
asymptomatic. The most clinically significant form of disseminated tuberculosis is miliary
disease, disease in 2 or more organs, which usually complicates the primary infection,
occurring within 2-6 mo of the initial infection. The clinical manifestations depend on the
load of organisms that disseminate and where they lodge. Lesions are often larger and more
numerous in the lungs, spleen, liver, and bone marrow than other tissues. systemic signs,
including anorexia ,weight loss, and low-grade fever are present. Generalized LAP and HSM
develop within several weeks. The fever can then become higher and more sustained.
Diagnosis: can be difficult, and a high index of suspicion by the clinician is required. Biopsy of
the liver or bone marrow often yields an early diagnosis. The most important clue is usually
history of recent exposure to an adult with infectious tuberculosis.
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 Central Nervous System Disease:
Presentation: The brain stem is often the site of greatest involvement→ dysfunction of
cranial nerves III, VI, and VII. can be divided into 3 stages
1st stage: 1-2 weeks ,characterized by nonspecific symptoms such as fever, headache,
irritability, drowsiness, and malaise. Prognosis is excellent for stage I.
2nd stage: The most common features are lethargy, nuchal rigidity, seizures, positive Kernig
and Brudzinski signs, hypertonia, vomiting, cranial nerve palsies, and other focal neurologic
signs.
3rd stage: coma, hemiplegia or paraplegia, hypertension, deterioration of vital signs, and
eventually death, survival with permanent disabilities with stage III.
Diagnosis: examination and culture of the CSF.
o Notes:
1-Other forms of TB are less significant or more rare.
2-systemic signs of weight loss , anorexia, fever , night sweats are almost always present in
every form of Tb , other signs refer to the location of infection ex:cough in pulmonary …etc.
o TREATMENT:
The standard therapy of TB is a 6 months regimen of isoniazid and rifampin supplemented in
the 1st 2 months of treatment by pyrazinamide and ethambutol.
therapy should continue to 9- 12 mo in :
For bone and joint, CNS, and disseminated TB, HIV infection.
Indications of steroids:
TB meningitis, Endobroncnhial TB, Miliary TB, and Pericardial TB. →Prednisone.
o Pharma
ANTITUBERCULAR DRUGS
-Combination drug therapy is the rule to delay or prevent the emergence of resistance and
to provide additive (possibly synergistic) effects against Mycobacterium tuberculosis.
-The primary (1st line) drugs in combination regimens are isoniazid (INH), rifampin(for the
whole 6months), ethambutol, and pyrazinamide(only in the first two months).
 Isoniazid
Mechanism: Prodrug requiring conversion by catalase. Inhibits mycolic acid synthesis.
-For bacilli in the stationary phase, INH is bacteriostatic, but for rapidly dividing organisms, it
is bactericidal.
-INH undergoes N-acetyaltion & hydrolysis, resulting in inactive products. In fast
acetylators→short half life, slow acetylators→long half life and excretion of the parent
drug(risk of SLE but rare).
adverse effects: Hepatitis, Peripheral neuritis (use vitamin B6), Mental abnormalities,
convulsions, optic neuritis & hyper sensitivity reactions.
Interactions: inhibitor of p450 system→ Isoniazid potentiates the adverse effects of
phenytoin.
 Rifampin
Mechanism: Inhibits DNA-dependent RNA polymerase (nucleic acid synthesis inhibitor).
-Rifampin is bactericidal for both intracellular & extracellular mycobacteria.
- Induction of P450→ decrease the t1/2 of the other drugs
- Red-orange metabolites (urine, feces and other secretions have orange-red color)
 Ethambutol
Mechanism :Inhibits synthesis of arabinogalactan (cell-wall component)
- Ethambutol is bacteriostatic
-The most important adverse effect is optic neuritis, which results in diminished visual
activity & loss of ability to discriminate between red & green.
 Pyrazinamide
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- bactericidal, antitubercular agent.
- Hepatitis → 1-5% of patients taking isoniazid, rifampin & pyrazinamide may experience
liver dysfunction.
- Hyperuricemia→ may precipitate a gouty attack.
 Problems with anti-TB drugs:

Side effects:
1- Dermatologic Adverse Effects: More with rifampin and also with INH especially when INH
taken with tyramine containing foods (cheese, red wine) or certain fish (tuna).
2- Gastrointestinal Adverse Effects: Nausea , vomiting and diarrhea, very commonly with
ethionamide, paraaminosalicylic acid (PAS) ,common with rifampin .
3- Hepatotoxicity: Caused by: INH + rifampin > INH alone >> pyrazinamide alone > rifampin
alone > ethionamide.
A . asymptomatic patients with an increase in LFTs from baseline:
1- if the increase in LFTs is < 3-5x normal: continue the current regimen and monitor for
symptoms of liver toxicity.
2- if the serum transaminases increases > 3-5x normal: hold INH until levels return to
baseline.
3- if the serum total bilirubin increases: therapy usually does not require modification
B.Symptomatic patients: hold drugs until symptoms resolve and the transaminases
decreases to < 2x normal. ethambutol and streptomycin should be started if drug therapy
can not be held .
4- Joints diseases: pyrazinamide>>ethambutol
5- influenza syndrome : More with rifampin
6- neurotoxicity (nervous system) Peripheral Neuropathy: INH>>>ethambutol, can be
treated with pyridoxine.
7- optic neuritis: ethambutol>>INH.
Resistance:
1- Monoresistant Mycobacterium Tuberculosis:
a-Isolated Resistance to ISONIAZID (INH).: treated with daily rifampin (RIF), ethambutol
(EMB), and pyrazinimide (PZA), all given for 6 to 9 months.
b-Isolated Resistance to RIFAMPIN (RIF): treated with INH, EMB, and a fluoroquinolone for
12 to 18 months, supplemented with at least 2 months of PZA.
c-Isolated Resistance to ETHAMBUTOL (EMB), PYRAZINAMIDE (PZA), or STREPTOMYCIN
(SM): little impact on the efficacy of the treatment regimen.
2- Polyresistant Mycobacterium Tuberculosis: resistance to more than one anti-TB drug (but
not INH and RIF) is referred to as polyresistant TB. Treatment should include the addition of
as many first line agents as possible plus a fluoroquinolone, and in some cases an injectable
drug(streptomycin).
3- Multidrug-Resistant Mycobacterium Tuberculosis (MDR-TB): defined as resistance to at
least INH and RIF. should always be treated with a minimum of 4 or more drugs to which the
isolate is susceptible..
Drugs interaction:
- Rifampin is enzyme inducer so can reduce plasma level of many drugs. → Increasing the
dose of these drugs may be required.
-INH is an enzyme inhibitor so reducing the dose of some drugs may be required.

A 42-year-old man comes to the emergency department because of fevers, fatigue, weight
loss, and cough for 3 weeks. He complains of fevers and a 4.5-kg weight loss. He describes
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his sputum as yellow in color. It has rarely been blood streaked. On physical examination, he
appears chronically ill with temporal wasting. There are amphoric breath sounds posteriorly
in the right upper lung field with a few scattered crackles in this area. He was diagnosed with
tuberculosis.
1-regarding the pathogenesis of his disease :

a-mycobacteria proliferate inside macrophages only.
b-ghon focus usually takes an apical position under high oxygen tension.
c-90% of initial Tb infection results in spread of organisims and disseminated disease.
d-it is immune mediated
e-primary infection is usually more severe than reactivation.
2- Which of the following virulence factors allows the causal agent to inhibit phagosome-
lysosome fusion to survive intracellularly?
(A) Cord factor(B) Calcium dipicolinate(C) Peptidoglycan(D) Sulfatides(E) Tuberculin
3- The most common means of transmission of Mycobacterium tuberculosis is:
a-Inhalation of organisms originating from soil or other environmental sources
b-Ingestion of organisms originating from soil or other environmental sources
c-Person-to-person spread by direct contact with infected discharge or contaminated fomite
d-Person-to-person spread by infected airborne droplets
4- All of the following factors infuence the likelihood of transmitting active tuberculosis
EXCEPT:
A. Duration of contact with an infected person
B. Environment in which contact occurs
C. Presence of extrapulmonary tuberculosis
D. Presence of laryngeal tuberculosis
E. Probability of contact with an infectious person
5-All of the following statements regarding BCG vaccination are true EXCEPT:
A. BCG dissemination may occur in severely immunosuppressed patients.
B. BCG vaccination is recommended at birth in countries with high TB prevalence.
C. BCG vaccination may cause a false-positive tuberculin skin test.
D. BCG vaccine provides protection for infants and children from TB meningitis and miliary
disease.
E. BCG vaccine provides protection from TB in HIV-infected patients
6- A 9 yr old child is found to have a positive PPD test result on routine screening. There are
no symptoms. Laboratory tests, including chest film, are normal. Which of the following is
the best interpretation of this finding?
a-Mycobacterium tuberculosis infection
b-Mycobacterium tuberculosis disease
c-Mycobacterium tuberculosis or atypical Mycobacterium infection
d-Mycobacterium tuberculosis or atypical Mycobacterium disease
e-Recent exposure to Mycobacterium tuberculosis but neither infection nor disease
7-A true statement concerning the 5-unit PPD skin test for tuberculosis is:
a-It is administered by subcutaneous injection
b-The reaction is measured 24 to 48 hr after administration
c-manifestation of type IV hypersensitivity
d-Corticosteroid therapy may increase the amount of reaction
e-Reaction is measured by the amount of erythema and induration
8-All of the following individuals receiving tuberculin skin PPD reactions should be treated
for latent tuberculosis EXCEPT:
A. A 23-year-old injection drug user who is HIV negative and has a 12-mm PPD reaction
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B. A 38-year-old fourth grade teacher who has a 7-mm PPD reaction and no known
exposures to active tuberculosis; she has never been tested with a PPD previously
C. A 43-year-old individual working in sub-Saharan Africa who has a 10-mm PPD reaction; 18
months ago, the PPD reaction was 3 mm
D. A 55-year-old man who is HIV positive and has a negative PPD; his partner was recently
diagnosed with cavitary tuberculosis
E. A 72-year-old man who is receiving chemotherapy for non-Hodgkin lymphoma and has a
16-mm PPD reaction
9-The recommended treatment for latent tuberculosis is:
a-Isoniazid for 6 mo
b-Isoniazid and rifampin for 6 mo
c-Isoniazid, rifampin, and pyrazinamide for 6-9 mo
d-Isoniazid and rifampin for 6 mo, with pyrazinamide and ethambutol added during the 1st 2
mo
e-Isoniazid and rifampin for 6 mo, with ethambutol during the first 2 mo
10-All of the following statements regarding interferon-γ release assays for the diagnosis of
latent tuberculosis are true EXCEPT:
A. There is no booster (repeated testing) phenomenon.
B. They are more specific than tuberculin skin testing.
C. They measure amount of INF- γ released in response to M.bovis antigens.
D. They have less cross-reactivity with BCG and nontuberculous mycobacteria than
tuberculin skin testing.
11-A 3 yr old child whose mother has tuberculosis has a positive PPD skin test result. A chest
film shows a localized, nonspecific infiltrate in the peripheral segments of the right lower
lobe. The most appropriate course of action to confirm the diagnosis of tuberculosis disease
in this child is:
a-Culture of sputum (induced with a jet nebulizer and chest percussion followed by
nasopharyngeal suctioning)
b-Culture of pulmonary secretions obtained by bronchoscopy
c-Culture of gastric contents obtained by gastric aspiration
d-Percutaneous lung and pleural biopsies for culture and histopathology
e-Segmental lobectomy for culture and histopathology
case scenario for 12-14
A 63-year-old woman comes to the physician because of a 2-week history of fatigue, and
decreased appetite; malaise, nausea and vomiting these symptoms have worsened during
the past week , She was diagnosed with tuberculosis 3 months ago, a multidrug regimen
was initiated at that time. Her temperature is 37.1°C (98.8°F). Physical examination shows
scleral icterus and tenderness over the right upper quadrant of the abdomen; there is no
hepatomegaly. serum studies show a total bilirubin concentration of 6.5 mg/dL, AST activity
of 580 U/L, and ALT activity of 650 U/L.
12- Which of the following drugs is the most likely cause of these finding ?
A) Ethambutol B) Isoniazid C) rifampicin D) Streptomycin (E) Pyrazinamide
13)In what way does the resistance to the inciting drug develop?
A. Decreased intracellular accumulation of the drug
B. Inactivation of the drug via N-acetyltransferases
C. Increased synthesis of mycolic acids
D. Mutations in the gene coding for DNA-dependent RNA polymerase
E. Reduced expression of the gene that encodes a catalase
14-What is the most appropriate action in this situation?
15-which of following statements regarding antituberculosis therapeutic agents is false ?
A. mycobacteria is termed poly-resistant if it shows resistance to rifampin and INH.
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B. Optic neuritis is the most severe adverse effect of ethambutol.
C. pyrazinamide can cause urate retention.
D. Rifabutin should be used instead of rifampin in patients receiving concurrent treatment
for HIV.
E. Rifampin can decrease the half-life of warfarin, cyclosporine, prednisone, oral
contraceptives, clarithromycin, and other important drugs.
o Notes in antibiotics
1-PRINCIPLES OF ANTIMICROBIAL CHEMOTHERAPY
Bacteriostatic drugs: arrest the growth & replication of bacteria thus limiting the spread of
infection while the body's immune system attacks, immobilizes & eliminates the pathogens.
Bactericidal drugs: kill bacteria, these agents are often the drugs of choice in seriously ill
patient(ex\patients with sepsis and septic shock )
Minimum inhibitory concentration (MIC) : is the lowest concentration of antibiotic that
inhibits bacterial growth.
Minimum bactericidal concentration (MBC): the MBC is the minimal concentration of
antibiotic that kills the bacteria.
Concentration- dependent killing: significant increase in the rate of bacterial killing as the
concentration of antibiotics increases from 4 to 64 fold the MIC of the drug for the infecting
organism(ex\ aminoglycosides & fluoroquinolones).
Post-antibiotic effect (PAE): persistent suppression of microbial growth that occurs after
levels of antibiotic have fallen below the MIC. Antimicrobial drugs exhibiting a
concentration-dependent killing and a long PAE often require only one dose per day.
Chemotherapeutic Spectra:
A. Narrow spectrum antibiotics: chemotherapeutic agents acting only on a single or a
limited group of microorganisms e.g. isoniazid.
B. Extended spectrum antibiotics: antibiotics that are effective against gram +ve organisms &
also against a significant number of gram -ve bacteria e.g. ampicillin.
C. Broad spectrum antibiotics: antibiotics that affect a wide variety of microbial species e.g.
tetracycline & chloramphenicol.
Antimicrobial combinations: 1. To provide broad spectrum empirical therapy 2. To treat
polymicrobial infections 3. To decrease the emergence of resistant strained 4. To decrease
dose related toxicity 5. To obtain enhanced inhibition or killing i.e. synergism
Note : Combinations:
Additive – Synergistic (penicillins plus aminoglycosides) or Antagonistic (penicillin
(bactericidal) plus tetracyclines (bacteriostasis)).
2- INHIBITORS OF CELL-WALL SYNTHESIS

-All cell-wall synthesis inhibitors are bactericidal
A. Penicillins
Mechanisms of action: Penicillins interact with cytoplasmic membrane-binding proteins
(PBPs) to inhibit transpeptidation reactions involved in cross-linking, the final steps in cell-
wall synthesis.
Subgroups and antimicrobial activity:
– Narrow spectrum, beta-lactamase sensitive: penicillin G and penicillin V
º Spectrum: streptococci, meningococci, Treponema pallidum,Clostridium perfringens,
Bacillus anthracis, Corynebacterium diphetheriae
– Very narrow spectrum, beta-lactamase resistant: nafcillin, methicillin, oxacillin
º Spectrum: known or suspected staphylococci (not MRSA)
– Extended spectrum, aminopenicillins, beta-lactamase sensitive: ampicillin and amoxicillin
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º Spectrum :antimicrobial spectrum similar to that penicillin G, but are more effective
against gram neg. bacilli. ampicillin includes gram +ve bacilli (listeria monocytogenes) and
gram -ve rods (Proteus mirabilis & Salmonella typhi while Escherichia coli and Haemophilus
influenzae are frequently resistant). Amoxicillin is employed prophytically by dentists for
patients with abnormal heart values who are to undergo extensive oral surgery.
–Extended spectrum, antipseudomonal, beta-lactamase sensitive: ticarcillin, piperacillin
º Spectrum: increased activity against gram-negative rods (except klebsiella) including
Pseudomonas aeruginosa, Piperacillin is the most potent of these antibiotic.
General considerations:
– Activity enhanced if used in combination with beta-lactamase inhibitors (clavulanic acid,
sulbactam)
– The antibacterial effects of all β-lactam antibiotics are synergistic with the
aminoglycosides.
Mechanisms of resistance:
– Penicillinases (beta-lactamases) break lactam ring structure (e.g., staphylococci)
– Structural change in PBPs (e.g., methicillin-resistant Staphylococcus aureus [MRSA],
penicillin-resistant pneumococci)
– Change in porin structure (e.g., Pseudomonas)
–Natural resistance:organisms that either lack a peptidoglycan cell wall e.g. mycoplasma or
have cell wall that are impermeable to the drugs.
Side effects:
− Hypersensitivity:Incidence 5 to 7% with wide range of reactions .Urticarial skin rash
common, but severe reactions, including anaphylaxis, are possible.
−GI distress(diarrhea): disruption of the normal balance of intestinal microorganisms ,
especially ampicillin>amoxicillin.
Rare side effects: Nephritis, Neurotoxicity, Hematologic toxicities, Cation toxicity.
B.Cephalosporins
−Mechanisms of action and resistance: identical to penicillins, except they are more
resistant to β-lactamases.
Subgroups and antimicrobial activity:
−Classified according to bacterial susceptibility patterns & resistance to β-lactamases
Organisms not covered by cephalosporins are “LAME”: Listeria monocytogenes, Atypicals
(e.g., Chlamydia, Mycoplasma), MRSA, Enterococci.
– First generation: cefazolin, cephalexin
º Spectrum: gram-positive cocci (not MRSA), E. coli, Klebsiella pneumoniae, and some
Proteus species
º Common use in surgical prophylaxis(cefazolin).
– Second generation: cefotetan, cefaclor, cefuroxime, cefoxitin
º Spectrum: ↑ gram-negative coverage, including some anaerobes.
Cefoxitin: in patients with intra abdominal sepsis & pelvic inflammatory disease(anaerobes)
Cefuroxime: only one that crosses BBB, used community acquired pneumonia.
– Third generation: ceftriaxone (IM) and cefotaxime (parenteral), cefdinir and cefixime (oral)
º Spectrum: gram-positive and gram-negative cocci (Neisseria gonorrhea), plus many gram-
negative rods
*Ceftriaxone: 1- with cefotaxime are agents of choice in the treatment of meningitis.
2- Neisseria gonorrhoeae drug of choice 3- empiric management of sepsis(g –ve)
4- Ceftriaxone has the largest half life of any cephalosporin (6-8hrs) 5- excreted in bile.
– Fourth generation: cefepime (IV)
º Even wider spectrum º Resistant to most beta-lactamases º Enters CNS
Pharmacokinetics:
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-Adequate therapeutic levels in the CSF, regardless of inflammation are achieved only with
3rd generation cephalosporins.
-Renal clearance similar to penicillins, with active tubular secretion→ Dose modification in
renal dysfunction.
Side effects:
- Hypersensitivity: Incidence: 2% →Wide range, but rashes and drug fever most common
Note : Assume complete cross-allergenicity between individual cephalosporins and partial
cross-allergenicity with penicillins (about 5%)
-Most authorities recommend avoiding cephalosporins in patients allergic to penicillins (for
gram-positive organisms, consider macrolides; for gram-negative rods, consider aztreonam).
-Other side effects: Disulfiram-like effect, Bleeding.
C. Carbapenems
Imipenem , meropenem and ertapenem are the only drugs.
Mechanism of action: Same as penicillins and cephalosporins
− Resistant to beta-lactamases
Spectrum: the broadest - spectrum β-lactam antibiotics preparations currently available.
− Important in-hospital agents for empiric use in severe life-threatening infections.
Pharmacokinetics: Imipenem is given with cilastatin, a renal dehydropeptidase inhibitor,
which inhibits imipenem’s metabolism to a nephrotoxic metabolite
Side effects:
− GI distress (vomiting & diarrhea).
− CNS effects, including seizures with imipenem in overdose or renal dysfunction
D. Monobactams:
Aztreonam is the only commercially available monobactam.
Mechanism of action:
− Same as for penicillins and cephalosporins
− Resistant to beta-lactamases
Uses:
− IV drug mainly active versus gram-negative rods(It has no activity against gram +ve
bacteria or anaerobe)
− No cross-allergenicity with penicillins or cephalosporins(safe alternative).
E.Vancomycin
Vancomycin inhibits synthesis of bacterial cell wall phospholipids as well as peptidoglycan
polymerization.
Spectrum:
– MRSA and MRSE (methicillin resistant S. aureus & epidermis).
– Enterococci : Vancomycin acts synergistically with aminoglycosides & this combination can
be used in the treatment of enterococcal endocarditis
– Clostridium difficile (backup drug)
Resistance:
− Vancomycin-resistant staphylococcal (VRSA) and enterococcal (VRE) strains emerging→
plasmid-mediated changes in the permeability to the drug or by decreased binding of
vancomycin to receptor molecules.
Pharmacokinetics: Used IV and orally (not absorbed) in colitis − Enters most tissues (e.g.,
bone), but not CNS − Eliminated by renal filtration (important to decrease dose in renal
dysfunction)
Side effects:
− “Red man syndrome” (histamine release)
− Ototoxicity (usually permanent, additive with other drugs)
− Nephrotoxicity (mild, but additive with other drugs)
−fever, chills & phlebitis at the infusion site
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Note : Daptomycin is used for treating infections caused by resistant gram positive
organisms, including MRSA and vancomycin -resistant enterococci(VRE).
3-INHIBITORS OF BACTERIAL PROTEIN SYNTHESIS

A. Aminoglycosides
Activity and clinical uses:

− Bactericidal, accumulated intracellularly in microorganisms via an O2-dependent uptake →
anaerobes are innately resistant
− Useful spectrum includes gram-negative rods; gentamicin, tobramycin, and amikacin often
used in combinations
Uses:
-Enterococcus species: gentamicin plus vancomycin or a β- lactam, such as penicillin-G
-Pseudomonas aeuroginosa: obramycin in combination with an anti-pseudomonal penicillin,
such as piperacillin or ticarcillin
-Klebsiella species: gentamicin plus an antipseudomonal penicillin .
-Brucella species: gentamicin or streptomycin plus doxycycline.
The antibiotic binds to the 30S ribosomal subunit and distorts its structure, thus interfering
with the initiation of protein synthesis. It also allows misreading of the mRNA, causing
mutations or premature chain termination.
Resistance:
when the oxygen dependent transport system or porin channels are absent,An altered 30S
ribosomal subunit, enzymes (e.g. acetyltransferase, nucleotidyltransferase,
phosphotransferase)
Pharmacokinetics:
-Are polar compounds, not absorbed orally→given parenterally.
-The bactericidal effect of aminoglycosides is concentration and time dependent.They also
have a post antibiotic effect→once-daily dosing .
Side effects:
1− Nephrotoxicity (6 to 7% incidence) includes proteinuria, hypokalemia, acidosis, and acute
tubular necrosis—usually reversible, but enhanced by vancomycin, amphotericin B, cisplatin,
and cyclosporine
2− Ototoxicity (2% incidence) from hair cell damage; includes deafness (irreversible) and
vestibular dysfunction (reversible), toxicity may be enhanced by loop diuretics and has been
known to affect fetuses in utero.
3-Neuromuscular blockade with ↓ release of ACh →intraperitoneal or intrapleural
application
4-contact dermatitis is a common reaction to topically applied neomycin.
B.Tetracyclines
− Bacteriostatic drugs, actively taken up by susceptible bacteria
− “Broad-spectrum” antibiotics
Uses:
1-drug of choice in infections with mycoplasma pneumonia, chlamydiae and rickettsiae
2-in combination with an aminoglycosides is indicated for brucellosis.
3-gastric and duodenal ulcer disease caused by helicobacter pylori
4-stop the shedding of vibrios in cholera
5-. Minocycline can eradicate the meningococcal carrier state.
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tetracyclines bind reversibly to the 30S subunit of the bacterial ribosome, blocking the
binding of aminoacyl-tRNA to the acceptor site on the mRNA-ribosome complex
Resistance:
Mg-depended active efflux of the drug, Enzymatic inactivation, proteins that prevent
tetracyclines from binding to the ribosome.
note: resistant strains may remain susceptible to doxycycline and minocycline.
Pharmacokinetics:
− urinary excretion for most (↓ dose in renal dysfunction)
− Liver for doxycycline→can be Used in renal dysfunction.
−Tetracyclines are classified as short action (chlortetracycline and tetracycline), intermediate
acting (demeclocycline), or long acting (doxycycline and minocycline).
Side effects:
1- GI distress and superinfections leading to candidiasis or colitis.
2- Tooth enamel dysplasia and possible ↓ bone growth in children (avoid)
3- Phototoxicity (demeclocycline, doxycycline)
4- Vestibular dysfunction (minocycline)
5- Have caused liver dysfunction during pregnancy at very high doses especially if they
were experiencing pyelonephritis (contraindicated).
6- Contraindications: a-renal impairment except doxycycline b- pregnant or breast
feeding woman c- children under 8 years of age.
C.Macrolides
Drugs: erythromycin, azithromycin, clarithromycin
− Macrolides are wide-spectrum bacteriostatic antibiotics.
o Erythromycin :
º Gram-positive cocci (not MRSA)
º Gram –ve organisms such as Neisseria , bordetella
º Atypical organisms (Chlamydia, Mycoplasma, Spirochetes)
o Azithromycin:
Azithromycin and erythromycin are virtually identical except azithromycin is :
-more active against respiratory infections due to H. influenzae and Moraxella catarrhalis.
-the preferred therapy for urethritis caused by Chlamydia trachomatis,active against
Mycobacterium avium-intracellulare (MAC), Less active against streptococci and
staphylococci.
Mechanism of Action:
The macrolides bind irreversibly to a site on the 50s subunit of bacterial ribosome, thus
inhibiting the translocation steps of protein synthesis.
Note: telithromycin(a ketolide) can be effective against macrolide resistant organisms.
Pharmacokinetics:
-Azithromycin is available for IV infusion
-Distributes well to all body fluids except the CSF, diffuse into prostatic fluid and it has the
unique characteristics of accumulating in macrophages
-They inhibit cytochrome P450s
-Primarily concentrated and excreted in an active form in the bile
Side effects:
1- GIT problems are their most common side effects (erythromycin> azithromycin >
clarithromycin).
2- reversible deafness at high doses
3- Cholestatic jaundice
4- Contraindications: patients with hepatic dysfunction should be treated with caution.
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5- Interactions: a-inhibit the hepatic metabolism of some drugs which can lead to toxic
accumulation of these compounds b- with digoxin:↑level
.D.Chloramphenicol
− Bacteriostatic with a wide spectrum of activity(Pseudomonas aeruginosa is not affected,
nor are the Chlamydiae)
− Currently a backup drug for infections due to Salmonella typhi, B. fragilis, Rickettsia, and
possibly in bacterial meningitis
Mechanism of Action:
binds to the bacterial 50s ribosomal subunit and inhibits protein synthesis at the peptidyl
transferase reaction
Pharmacokinetics:
− Orally effective, with good tissue distribution, including CSF
− Metabolized by hepatic glucuronidation, and dose reductions are needed in liver
dysfunction and in neonates
− Inhibition of cytochrome P450
Side effects:
1-Dose-dependent bone marrow suppression common(Reversible anemia); aplastic anemia
rare →idiosyncratic(independent of dose)
2-Hemolytic anemia occurs in patients with low levels of glucose-6- phosphate
dehydrogenase
3-“Gray baby” syndrome in neonates (↓ glucuronosyl transferase) →depressed breathing,
cardiovascular collapse, cyanosis and death.
4-GIT upsets. 5- Overgrowth of Candida albicans .
E.Clindamycin
Not a macrolide, but has the same mechanisms of action and resistance,Clindamycin is
employed primarily in the treatment of infections caused by anaerobic bacteria, such as
Bacteriodes fragilis &active against non-enterococcal gram +ve cocci.
The most serious adverse effect is potentially fatal pseudomembranous colitis caused by
overgrowth of Clostridium difficile.
F.Quinupristin–Dalfopristin
Spectrum:
Used parenterally in severe infections caused by vancomycin-resistant staphylococci (VRSA)
and enterococci (VRE), as well as other drug resistant gram-positive cocci, bacteriostatic.
Adverse effects: include venous irritation, arthralgia and hyperbilirubinemia.
G.Linezolid
Uses: resistant gram +ve organisms, such as methicillin and vancomycin resistant
Staphylococcus aureus, vancomycin-resistant Enterococcus faecium and Enterococcus
faecelis, and penicillin-resistant streptococci.
Notes :
1- Quinupristin–Dalfopristin for E. faecium, including VRE faecium, but not for E.
faecalis ,Linezolid for both types of enterococci
2- Don’t Use in Pregnancy! Aminoglycosides, fluoroquinolones, sulfonamides,
tetracyclines
4-INHIBITORS OF NUCLEIC ACID SYNTHESIS

A.Quinolones
Drugs: ciprofloxacin, levofloxacin, and other “−floxacins”
Mechanisms of action:
Quinolones are bactericidal and interfere with DNA synthesis
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− Inhibit topoisomerase II (DNA gyrase) and topoisomerase IV (responsible for separation of
replicated DNA during cell division)
− Urinary tract infections (UTIs),particularly when resistant to cotrimoxazole
(ex:Pseudomonas.)
− Sexually transmitted diseases (STDs)/pelvic inflammatory diseases (PIDs): chlamydia,
gonorrhea
−Bacterial Diarrhea caused by Shigella, Salmonella, toxigenic E. coli or Campylobacter
−Typhoid fever(drug of choice)
−Prophylaxis and treatment of Anthrax.
Pharmacokinetics:
-Iron, calcium limit their absorption − Eliminated mainly by kidney
Adverse Effects:
1-Gastrointestinal, the most common, nausea and vomiting
2-CNS effects (insomnia, dizziness, headache)
3-Photosensitivity
4-Connective tissue problems:
– Tendonitis, tendon rupture
–Possibility of inhibition of chondrogenesis in children with cystic fibrosis who receive
ciprofloxacin.
5-Contraindications: moxifloxacin prolong the QT interval and, thus, should not be used in
patients who are predisposed to arrhythmias.
B.Inhibitors of Folic Acid Synthesis
1-Sulfonamides
Mechanism of action: Sulfonamides inhibit Dihydropteroate synthetase. The sulfa drugs,
including co-trimoxazole are bacteriostatic.
Spectrum:
Sulfa drugs are active against selected enterobaceria in the urinary tract and nocardia.
Pharmacokinetics:
a- Oral absorbable agents:
1. Short acting agents, e.g. sulfisoxazole.
2. Medium acting agents, e.g. sulfadiazine, sulfamethoxazole.
*sulfadiazine+pyrimethamine →toxoplasmosis
3. Long acting agents, e.g. sulfadoxine. *sulfadoxine+pyrimethamine=(Fansidar) malaria
b-Oral non-absorbable agent : Sulfasalazine used in ulcerative colitis and rheumatoid
arthritis
c- Topical agents : Ag sulfadiazine used in burns, sodium sulfacetamide in bacterial
conjunctivitis
Adverse effect:
1. Crystalluria →alkalinization of urine prevent the problem.
2. Hypersensitivity (rashes, Stevens-Johnson syndrome)
3. Hemolysis in G6PD deficiency
4. Kernicterus: in newborns because of sulfa drugs displace bilirubin from binding sites
on serum albumins
5. Contraindications: newborns and infants less than two months of age, as well as for
pregnant women at term→ Kernicterus
2- Trimethoprim
inhibitor of bacterial dihydrofolate reductase has a spectrum similar to that of
sulfamethoxazole. It can produce the effects of folic acid deficiency. These effects include
megaloblastic anemia, leukopenia, and granulocytopenia. These blood disorders can be
reversed by the simultaneous administration of folinic acid.
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Co-trimoxazole:
The combination of trimethoprim with sulfamethoxazole (ratio 1.5).
º Bacteria: Gram-negative infections (E. coli, Salmonella, Shigella, H. influenzae) so used in
urinary tract infections, Respiratory infections, GIT infections and systemic salmonella.
DOC in Nocardia (you are going to take it in mycology)
º Fungus: Pneumocystis jiroveci
test your self part -7-

Q1\Match each class of antibiotic with its mechanism of action.
1- Ampicillin.2- Azithromycin. 3- Ciprofoxacin.4- Tobramycin 5- sulfamethoxazole
A. Binds to 30S ribosomal subunit inhibiting initiation of protein synthesis
B. Binds to 50S ribosomal subunit and inhibits protein synthesis at the peptidyl transferase
reaction
C. Inhibits cell wall synthesis by binding to transpeptidase enzymes involved in peptide cross-
linking
D. Inhibits DNA gyrase and topoisomerase to inhibit DNA synthesis
E. Inhibits bacterial dihydrofolate reductase
F. Binds to 50S ribosomal subunit inhibiting the translocation steps of protein synthesis
G.Binds to 30S ribosomal subunit blocking the binding of aminoacyl-tRNA to the acceptor
site on the mRNA
H.Inhibits bacterial dihydrofolate synthetase
Q2\Match each antibiotic with its side effect.

Note : choose all that apply.
List 1
1-gentamicin 2-chloramaphenicol 3-vancomycin 4-clindamycin 5-sulfonamides
6-ciprofloxacin 7-ampicillin 8-tetracycline
List 2
a-pancytopenia b-hepatotoxcicity c-nephrotoxcicity d-GI adverse effects
e-hypersensitivity f-ototoxcicity g-pseudomembranous colitis
h-red man syndrome i-crystalluria j-hypersensitivity
k- CNS effects (insomnia, dizziness, headache l-gray baby syndrome
m-bone growth in children.
Prepared by :
Haitham nabeel
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 Sepsis and septic shock

o Definitions:
• Bacteraemia: the presence of viable bacteria in the bloodstream
Diagnostic criteria : Positive blood culture, pneumococcus is the most common organism to
cause bacteremia.
• Septicemia : proliferating bacteria in the blood.
• SIRS: Systemic Inflammatory Response Syndrome : Inflammatory response to infective and
non infective causes such as pancreatitis, vasculitis, trauma.
Diagnostic criteria : Defined by ≥ 2 of:
1– Temp > 38C or < 36C
2–HR > 90 bpm
3– RR > 20 / min or PaCO2 < 32 mmHg (< 4.3 kPa)
4 –WBC > 12 x 109/L or < 4 x109/L or or > 10% immature (band) forms.
• Sepsis: systemic inflammatory response to proven or suspected infection.
Diagnostic criteria: SIRS+ suspected or proven infection.
• Severe sepsis : sepsis + organ dysfunction or hypotension.
Diagnostic criteria: sepsis +( SBP ≤90mmHg or 40 mmHg less than patient's normal BP) or
sign of organ dysfunction for example • Jaundice • Bruising or intense bleeding. •
Decreased urination. • Peripheral edema. • Signs of heart failure. • Respiratory alkalosis and
metabolic acidosis. •altered mental status,confusion (suggestive of brain hypoperfusion)
•septic shock : severe sepsis plus the persistence of hypoperfusion or hypotension despite
adequate fluid resuscitation or a requirement for vasoactive agents.
Diagnostic criteria: severe sepsis+ unresponsiveness to fluid resuscitation.
• MODS: Multiple Organ Dysfunction Syndrome : Impaired organ function in critically ill
patient with SIRS. If not treated then multiple organ failure and death.
 Pediatrics
History: Includes fever, poor feeding or appetite, lethargy or fatigability plus history of focal
infection.
Clinical manifestations:
-The initial signs and symptoms of sepsis include alterations in temperature regulation
(hyperthermia or hypothermia), tachycardia, and tachypnea.
-Early stage “warm” shock : the cardiac output increases →hyperdynamic circulation.
-Late stage “cold” shock: As septic shock progresses, cardiac output falls in response to the
effects of numerous inflammatory mediators, leading to a compensatory elevation in
systemic vascular resistance
-signs of poor cardiac output include: delayed capillary refill, diminished pulses, cool
extremities, and decreased urine output, alteration in mental status (confusion, agitation,
lethargy, or coma).
-Cutaneous lesions seen in septic patients include petechiae and ecchymosis, Jaundice can
be seen either as a sign of infection or as a result of MOD.
Diagnosis: SIRS in the presence of proven infection or clinical picture consistent with
infection. Physical examination plays a role in the diagnosis.
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- An infectious etiology should be sought including culturing body fluids (blood, urine,
cerebrospinal fluid, abscesses and peritoneal fluid).
Laboratory abnormalities:
1-Hematological changes : thrombocytopenia, leukopenia or leukocytosis, anemia,
prolonged prothrombin time and partial thromboplastin time, reduced serum fibrinogen
level and elevated fibrin split products.
2-Electrolytes abnormalities: hyperglycemia or hypoglycemia, hypocalcemia,
hypoalbuminemia, and metabolic acidosis.
3- Renal and liver function tests are impaired if the patient develops MOD.
Treatment:
Broad spectrum bactericidal synergistic antimicrobial agents should be promptly
administered to the patient. the choice is dependent on the predisposing factors and the
clinical situation.
Supportive care:
1- fluid resuscitation : in significant hypovolemia
2- Vasopressor and inotropic agents to maintain cardiac output
3- Blood and blood products can be used if the patient has active bleeding or DIC
4- vital signs , metabolic and renal monitoring.
 Medicine
Clinical Signs of Sepsis: • Fever. • Leukocytosis or leukopenia. • Tachypnea. • Tachycardia.
• Organ Dysfunction.
Clinical Signs of Septic Shock: • Myocardial Depression. • Altered Vasculature. • Altered
Organ Perfusion. • Imbalance of O2 delivery and Consumption. • Metabolic (Lactic) Acidosis
Basic and early investigations are: • WBC. • Serum lactate. • Blood culture and culture of
respiratory secretions. • Renal and liver functions. • Clotting screen. • CXR.
Laboratory Findings • leukocytosis with a left shift or leukopenia. • Thrombocytopenia.
• Hyperbilirubinemia. • Proteinuria. • Prolongation of the thrombin time, decreased
fibrinogen, and the presence of d- dimers, suggesting disseminated intravascular coagulation
(DIC.) • Azotemia. • Hypoxemia, respiratory alkalosis. • Metabolic acidosis.
Resuscitative measures(sequence of first 3 is imp.):
• High-flow oxygen. • Intravenous fluids (crystalloids) with monitoring of HR, BP and urine
output. • Systemic broad spectrum antibiotic(ideally within 1 hour and after cultures taken).
• Ensuring adequate nutrition (enteral or parenteral.) • Control of blood sugar by insulin.
• Hemodialysis in kidney failure. • Mechanical ventilation. • Transfusion of blood products.
• Medication to prevent DVT and gastric ulcer may also be used.
Therapeutic goals
• Central venous pressure: 8 – 12 mmHg
• Mean arterial pressure: ≥ 65 mmHg
• Urine output: 0.5mL/kg/h
• Central venous or mixed venous oxygen saturation: ≥ 70%
Fluid Therapy
administration of IV beginning with crystalloid , The urine output rate should be kept at >0.5
ml/kg /h. colloids should be given to assess BP response to volume.
Vasoactive drugs
1-noradrenaline or dopamine for increasing SVR and BP
2- dobutamine is necessary to maintain CO
Markers of perfusion
• Clinical signs: Warm skin, conscious level, urine output.
• Hemodynamic variables: Central venous pressure (CVP.)
• Blood: Serum Lactate→ 1> normal , 1-2 is a concern, >2 is bad, 4<is very bad.
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Bacteriology 2017
 Surgery
qSOFA: quick Sepsis Related Organ Failure Assessment
2 of 3 of the following :
1-Low blood pressure (SBP ≤ 100 mmHg)
2- High respiratory rate ( RR ≥ 22 breaths/min)
3-Altered mentation (GCS < 15)
A 70-year-old man presents to the emergency department with a 2- day history of fever,
chills, cough and right- sided pleuritic chest painThe patient’s vital signs are:
Temperature 39C°; heart rate 120 bpm; respiratory rate 30 breaths/min; blood pressure
70/35 mmHg; and oxygen saturation 80% without oxygen supplementation. A chest
radiograph shows a right lower lobe infiltrate and diagnosed as pneumonia.
1. This patient’s condition can best be defined as which of the following?
(A) Multiorgan dysfunction syndrome
(B) Sepsis
(C) Septic shock
(D) Severe sepsis
(E) Systemic inflammatory response syndrome
2. After ensuring adequate airway and oxygenation, what is the next step in the
management of this patient?
(A) Antibiotic therapy
(B) β-Blocker therapy to control heart rate
(C) Intravenous fluid resuscitation
(D) Surgical consultation
(E) Vasopressor therapy with dopamine
3.In the treatment of septic shock, what is the goal for urine output?
(A) Urine output ≤ 0.3 mL/kg/hr
(B) Urine output ≥ 0.2 mL/kg/hr
(C) Urine output ≥ 300 mL per day
(D) Urine output ≥ 0.5 mL/kg/hr
4-All of the following are components of early goal directed therapy (EGDT) in the
resuscitation of this patient with severe sepsis/septic shock EXCEPT:
(A) IV fluid resuscitation targeting CVP 8 to 12 cm H2O
(B) IV vasopressor infusion to maintain SBP > 90 Hg
(C) IV vasopressor infusion to maintain MAP > 65 mm Hg
(D) Central venous or mixed venous oxygen saturation: ≥ 70%
5-Which one of the following is not a parameter in the definition of SIRS?
a. Hypotension
b. Tachycardia
c. Tachypnea
d. Leukocytosis
e. Hypothermia
6-Which is an early finding in septic shock?
a. Decreased urine output c. Decreased blood pressure
b. Increased cardiac output d. Diffuse lung infiltrates
Prepared by :
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Bacteriology 2017
Haitham nabeel
 Surgery notes
Surgical infection
Factors that determine whether a wound will become infected • Host response • Virulence
and inoculum of infective agent •Vascularity and health of tissue being invaded (including
local ischaemia as well as systemic shock) •Presence of dead or foreign tissue •Presence of
antibiotics during the ‘decisive period’.
-Surgical wound infection can lead to local (cellulitis, lymphangitis, abscess) and systemic
(bacteremia) complications.
-The infection of most surgical wounds is referred to as superficial surgical site infection
(SSSI). While Deep SSI (infection in the deeper musculofascial layers) and organ space
infection (such as an abdominal abscess).
Major SSI
wound that either discharges significant quantities of pus spontaneously or needs a
secondary procedure to drain it. Associated with Delayed return home and Patients are
systemically ill.
Minor wound infections may discharge pus or infected serous fluid but should not be
associated with excessive discomfort , systemic signs or delay in return home.
o TYPES OF LOCALIZED INFECTION:

1-ABSCESS:
-clinical features of acute inflammation: • Calor (heat), • Rubor (redness), • Dolor (pain), •
Tumour (swelling). • To these can be added (Loss of Function).
-Caused by Pyogenic organisms, predominantly Staphylococcus aureus.
-Management :
-Abscesses need drainage. No need for antibiotic, if the cavity is left open to drain freely.
Antibiotics are indicated if the abscess is not localised (e.g. evidence of cellulitis) or the
cavity is not left open to drain freely. Modern imaging techniques may allow guided
aspiration.
-If it is not drained or reabsorbed completely, a Chronic Abscess may result. If it is partly
sterilized with antibiotics, an Antibioma may form. If they spread, they usually track along
planes of least resistance and point towards the skin.
-Certain organisms are associated with chronicity, sinus and fistula formation. Common ones
are: Mycobacterium and Actinomyces.
2-CELLULITIS AND LYMPHANGITIS:
-Cellulitis is the non-suppurative invasive infection of tissues. There is poor localization in
addition to the cardinal signs of inflammation.
-Systemic signs (toxaemia): fever, sweating, and rigors (chills).
-Commonly caused by streptococci, staphylococci or clostridia, Blood cultures are often
negative. Lymphangitis is part of a similar process and presents as painful red streaks in
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Bacteriology 2017
affected lymphatics. ,Lymphangitis is often accompanied by painful lymph node groups in
the related drainage area.
o Systemic presentation:
bacteremia and sepsis (already discussed).
o SPECIFIC WOUND INFECTIONS

Gas gangrene: caused by C. perfringens, relevant to military and traumatic surgery and
colorectal operations, Immunocompromised ,diabetic or have malignant disease are at
greater risk, associated with severe local wound pain and crepitus. (gas in the tissues noted
on plain radiographs).
Antibiotic prophylaxis should always be considered in patients at risk.
• intravenous penicillin and aggressive Debridement of affected tissues are required.
• Amputation stump is covered by flufly bandage to prevent faecal contamination with
clostridia spores.
Clostridium tetani:
Trismus, risus sardonicus ,opisthtonos and dyspnea.
Prophylaxis with tetanus toxoid is the best preventative treatment.
• In infection minor debridement of the wound.
• antibiotic treatment with benzyl penicillin
NECROTIZING FASCIITIS:
mixed pattern of organisms is responsible. Almost always immunocompromised.
• Severe wound pain, signs of spreading inflammation with crepitus and smell.
Abdominal wall infections are known as Meleney’s synergistic hospital gangrene.
• Scrotal infection as Fournier’s gangrene.
Broad spectrum antibiotics and circulatory support with debridement and wide excision.
Principles for the use of antibiotic therapy
1- Antibiotics do not replace surgical drainage of infection
2- Only spreading infection or signs of systemic infection justifies the use of antibiotics
3- Whenever possible, the organism and sensitivity should be determined
o Hospital acquired infection

An infection is considered nosocomial if they first appear 48 hours or more after hospital
admission or within 30 days after discharge from hospital.
Most common sites in order of frequency are :
1-UTI 2- surgical site infection 3- lower respiratory 4-cutaneous infections 5-bacteremia
Sources of infection
(a) Endogenous: patient own flora
(b) Exogenous: from another patient, staff member, and environment of hospital or
from environmental sources
Staphylococcus aureus is the most common organism to infect the surgical wound.
Wound infection in relation to source of sepsis:

1-Operating theater: 1st seen at 1st dressing, May not be a deep infection, bacteria are
Usually unique and reflect source of infection.
2-ward: appears After 1st dressing or after 3-4 days postoperative , Usually superficial, her
patients will usually have the same or similar type of causative bacteria.
the most significant variable in the acquisition of wound infection is the type of
operation and whether this starts initially as a clean or contaminated one.
Type of operation
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Bacteriology 2017
1-Clean operations : No viscus opened, less than 2% risk. Ex\ herniotomy repair, excision of
lipoma, skin biopsy, excisional biopsy of lymph node , excision of breast fibroadenoma,
surgery on meninges and brain, joint, eye, heart, peripheral vessels and transplant surgery.
2-Clean Contaminated operation : Viscus opened ,minimal spillage , Less than 10% risk.
Ex\ appendeciectomy, cholecystectomy, surgery on vagina,, and also for trauma.
3-Contaminated : Open viscus with spillage or inflammatory disease. 15-20% risk.
Ex\ Perforated appendix, resection of unprepared bowel
4-Dirty : Pus or perforation, or incision over abscess. 28%-70% risk.
Ex\ Drainage of abscess, as perianal ischeorectal, surgery on infected joint, pyosalpinx,
empyema of the gall bladder.
the commonest surgical opportunists are gram-negative organisms of which the

most frequent are E. coli, pseudomonas species, klebsiella, proteus, and serratia
Of the gram positive opportunist infections staph. Epidermidis is most frequently
found.
combination of a broad spectrum as third generation cephalosporin and
metronidazole parenteral will produce a response of majority of patients as these
drugs cover G+ and G- and bacteroids.
o Gangrene
The death of body tissue due to the loss of blood supply to that tissue, sometimes
permitting bacteria to invade it and accelerate its decay.
-Classification: • Primary gangrene • Secondary gangrene
-Primary gangrene(gas gangrene): caused by clostridium perfiringes. (discussed).
-Secondary gangrene: can be classified into 1-dry gangrene 2-wet gangrene.
1-dry gangrene:
-Dry gangrene begins at the distal part of the limb due to ischemia and often occurs in the
toes and feet of elderly patients due to arteriosclerosis.
-Dry gangrene spreads slowly until it reaches the point where the blood supply is adequate
to keep tissue viable. The affected part is dry, shrunken and dark black, resembling
mummified flesh. The early signs are a dull ache and sensation of coldness in the affected
area.
-Due to gradual cut of blood supply. The line of demarcation between dead and living tissue
is clear. The lesion remains localized. Affected body parts feel cold and turn dark, it will dry
and eventually falling off .If caught early, the process can sometimes be reversed by vascular
surgery.
2-wet gangrene:
-It occurs in internal organs where moisture and temperature are favorable for bacterial
growth. The affected part is soft, putrid, rotten and dark. The infected tissue are edematous
due to large amount of subcutaneous fluid. The demarcation between dead and living is
indistinct. May extend proximally beyond the site of infection.
-The toxic products formed by bacteria are absorbed causing systemic manifestation of
bacteremia and finally death.
-Bedsores occurring on body parts such as the sacrum, buttocks and heels (not in “moist”
areas) are also categorized as wet gangrene infections.
 SPECIFIC GANGRENES
-NOMA: a is a gangrene of the face, especially the mouth and cheek. Risk factors include
severe protein mal nutrition and unsanitary conditions.
-NECROTIZING FASCIITIS: flesh-eating disease or flesh-eating bacteria, infection of the
deeper layers of skin and easily spread within the subcutaneous tissue.
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Bacteriology 2017
-FOURNIER GANGRENE: affects the male genitals, In the majority of cases it is a mixed
infection caused by both aerobic and anaerobic bacteria.
 TREATMENT :
-The method of treatment is generally determined depending on location of affected tissue
and extent of tissue loss.
-Usually surgical with amputation necessary in many cases.
-The best treatment for gangrene is revascularization and restoration of blood flow to the
affected area, Can reverse some of the effects of necrosis and allow healing.
-Antibiotics alone are not effective because they do not penetrate ischemic muscles
sufficiently.
Test yourself
Note: in this test more than one answer could be correct please select all that
apply.
You need to study the whole lectures to answer them not only the notes.
1-Which of the following is a risk factor for wound infection?

A-Poor perfusion
B-Use of skin clips for wound closure.
C-Poor surgical technique
D-Not using prophylactic antibiotics
E-Uraemia
2-Which of the following statements about surgical site infections (SSIs) are true?
A-Infection in the musculofascial tissues is known as deep SSI.
B-The patient may have systemic signs in a minor SSI.
C-Infection causing delay in hospital discharge is a major SSI.
D-The differentiation between major and minor SSIs is not important.
E-The best example of deep SSI is abdominal abscess after anastomotic leak.
3-Which of the following statements regarding abscesses are true?
A-Staphylococcus aureus is one of the most common causative organisms.
B-The abscess wall is composed of epithelium.
C-Most wound-site abscesses occur before the patient is discharged from the hospital.
D-Antibiotics are indicated if there is evidence of cellulitis.
E-Actinomyces can cause a chronic abscess.
4-Which of the following statements regarding cellulitis are true?
A-This is non-suppurative invasive infection of tissues.
B-It is poorly localised.
C-It is commonly caused by Clostridium perfringens.
D-Systemic signs are not present.
E-Blood culture is usually positive
5-Which of the following statements regarding clostridial wound infections are true?
A-Clostridia are Gram-positive aerobic spore-bearing cocci.
B-Thin, brown and sweet-smelling exudates is seen in gas gangrene.
C-Necrotic and foreign material in wounds increase risk.
D-The spores are widely spread in soil.
E-The signs and symptoms are due to the endotoxins.
6-Which of the following affects the choice of prophylactic antibiotic?
A-The expected spectrum of organisms likely to be encountered
B-Cost
C-Personal preference
D-Hospital policies
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Bacteriology 2017
E-Local resistance strains
7-Which of the following statements about types of wounds are true?
A-The infection rate in a ‘clean wound’ is between 1 and 2 per cent.
B-The wound after a biliary surgery is classified as ‘contaminated’.
C-A ‘clean-contaminated wound’ has an infection rate of less than 10 per cent.
D-Antibiotic prophylaxis would be mandatory in ‘dirty wounds’.
E-The role of prophylactic antibiotics in non-prosthetic clean surgery is controversial.
8-Which of the following statements regarding antimicrobial treatment of surgical infections
are true?
A-Antibiotics are mandatory in all SSIs.
B-Antibiotics should not be started before knowing the causative organism and sensitivity.
C-A ‘broad-spectrum’ approach is used while treating methicillin-resistant Staphylococcus aureus
(MRSA) infections.
D-Antibiotics can be used as a replacement for surgical drainage.
E-Rotating antibiotics may be required in the treatment of ‘resident opportunists
Match the type of wound with corresponding matches
A-Clean
B-Clean-contaminated
C-Contaminated
D-Dirty.
1-Drainage of an abscess
2-No viscus opened
3-Gastric and biliary surgery
4-Wound infection rate 1–2 per cent
5-Open viscus surgery or gross spillage or inflammatory bowel disease
6-Wound infection rate 15–20 per cent
7-Wound infection rate < 40 per cent
8-Wound infection rate < 10 per cent.
Prepared by :
Haitham nabeel
64
Bacteriology 2017
 Food poisoning
Important considerations:
1-Presenting symptoms : you cannot usually diagnose a patient with food poisoning from
symptoms only as they are similar but they help to differentiate and in some cases they
provide a clue to Dx. for example : Bloody stools+ fever suggest shigellosis but confirmation
is required.
2- Exposure to a particular type of food associated with foodborne disease: for ex:rice and
B.cereus or salad dressings with S.aureus. (they are mentioned in community part)
3-The time interval between exposure to the suspect food and the onset of symptoms:
Can be classified into 3 categories.
a-preformed toxins: IP is usually between 6-12 hrs. symptoms are predominately upper
intestinal(vomiting is the major symptom). They include: Staphylococcus aureus, Bacillus
cereus emetic toxin and botulism.
b-Pathogens that make toxin once they have been ingested: IP is usually 24 hours or longer.
causes non inflammatory diarrhea that may be watery in Vibrio cholera, C perfringens or
ETEC or bloody in EHEC.
Note : non-inflammatory diarrhea is a diarrhea that is not associated with systemic
manifestations like (fever, bacteremia) or presence of PMNs(pus) cells in stool.
c-invasive microbes: IP is usually days. produce a wide spectrum of clinical presentations
from watery diarrhea (eg, Cryptosporidium parvum, enteric viruses) to inflammatory
diarrhea (eg, Salmonella, Campylobacter, Shigella,EIEC) or systemic disease (eg, L.
monocytogenes)
inflammatory diarrhea : diarrhea associated with fever and presence of WBCs in stool.
Diagnosis:
Tests that may help include:
1-Stool Gram staining for WBCs: To help differentiate invasive disease from noninvasive
disease
2-Bacterial culture for enteric pathogens: mandatory if positive results for WBCs or blood,
patients have fever or symptoms persisting for longer than 3-4 days
3-Blood culture in febrile patients
4-Microscopic examination of the stool: To detect any ova and parasites
5-C difficile assay
Treatement:
primarily supportive.
1-adequate rehydration with ORS or intravenous in severely dehydrated.
2-Antibiotics are recommended for some, but not all types of food poisoning. Selection of
antibiotic depends on clinical setting and guided by microbiology and blood culture
sensitivity results.
3-Antidiarrheals can prolong these illnesses and are not generally recommended .
4-Patients should avoid milk, dairy products, and other lactosecontaining foods→ temporary
lactose intolerance.
65

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Sepsis and septic shock 57

GRAM POSETIVE COCCI

1. Streptococcus pyogenes (Group A Streptococcus; GAS)

o Distinguishing Features bile insoluble

5-All of the following are features of scarlet fever EXCEPT:

Question 11 refer to the following case:

12)What is the most likely mechanism of resistance for methicillin-resistant staphylococcus

Test youself part-2-

GRAM POSETIVE BACILLI

Distinguishing Features -Floppy baby syndrome (infant with

Test yourself part-3

Case scenario for question 10

GRAM NEGATIVE BACILLI

Trans- Mechanism of Clinical Clues Treatment

1- UTI (most Endogenous Motility Gram (−) bacilli, Fluoroquinolone

o Urinay tract infections.

 CLINICAL MANIFESTATIONS • High swinging undulating temperature (hence named

 DIAGNOSIS : Non-specific Lab Tests • CBC→WBC are usually normal to low;

Diagnosis : mainly clinical especially in outbreaks. In laboratory confirmation follow the

Test yourself part-4-

2)All of the following is true regarding the causative agent except :

3)Which of the following statements regarding vibriosis is false?

4) What is the most appropriate treatment for our patient?

Case scenario for questions 5-6

5)virulence factor of the causal agent is most important to pathogenesis?

Case scenario for questions 7-9

 Chlamydia Dx: 1- cell culture 2- Chlamydial antigens can be detected by ELISA

Test yourself part-5-

6)Upon delivery, what complication is her infant most at risk for?

o Now let's follow TB bacilli in their journey inside the body!

 Problems with anti-TB drugs:

Test yourself part-6-

1-regarding the pathogenesis of his disease :

2- INHIBITORS OF CELL-WALL SYNTHESIS

3-INHIBITORS OF BACTERIAL PROTEIN SYNTHESIS

Activity and clinical uses:

4-INHIBITORS OF NUCLEIC ACID SYNTHESIS

test your self part -7-

Q2\Match each antibiotic with its side effect.

 Sepsis and septic shock

o TYPES OF LOCALIZED INFECTION:

o SPECIFIC WOUND INFECTIONS

o Hospital acquired infection

Wound infection in relation to source of sepsis:

the commonest surgical opportunists are gram-negative organisms of which the

1-Which of the following is a risk factor for wound infection?

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