Neisserial infections Whooping cough Pseudomonas infections Plague Chancroid (soft chancre) Granuloma inguinale

1. Gram negative bacterial infections
1. Neisserial infections
2. Whooping cough
3. Pseudomonas infections
4. Plague
5. Chancroid (soft chancre)
6. Granuloma inguinale

2. Neisseriae
• Gram negative diplococci.
• Two clinically significant Neisseria
are:
1. N.meningitidis (meningococcus)
2. N.gonorrhoeae (gonococcus)

3. N.meningitidis
• Meningococcal disease:
– Meningitis
– Fulminant Meningococcemia (purpura fulminans)
– Waterhouse-Friderichsen Syndrome
• Virulence factors
• Capsule
– Reduces opsonization and destruction of
bacteria by complement proteins.
– High rates of disease in people with
complement deficiency.
• Endotoxin (LPS)
–

4. Pathology and pathogenesis

5. • Initial colonization of nasopharynx 
asymptomatic meningococcal Pharyngitis.
• Invades the epithelial cells and enters the
blood (bacteremia) :
– Can result in :
• Meningococcemia (purpura fulminans)
• Waterhouse-Friderichsen syndrome
• Meningitis

6. Purpura fulminans (meningococcemia)
• Due to intravascular multiplication of
organisms.
– Produces septic shock and DIC
• Clinically Characterized by: Hemorrhagic
skin lesions (purpura), spiking fever, chills
and hypotension.
• Dissemination can result in Meningitis or
Waterhouse-Friderichsen syndrome

7. Meningococcemia
Petechial hemorrhages Skin Purpura

8. Waterhouse-Friderichsen Syndrome
• This uncommon but catastrophic syndrome seen
mainly in very young children.
• Due to overwhelming infection by N.meningitidis
• C/F:
– Hypotension leading to shock
– DIC induced microthrombosis , hemorrhage
and tissue injury.
– widespread purpura, particularly of the skin
– Bilateral adrenal hemorrhage 
adrenocortical insufficiency .

9. Patient with waterhouse-friderichsen syndrome

10. A
B

11. Meningitis
• Most common form of disease.
• Transmitted by droplet nuclei
• The organisms usually colonize nasopharynx.
• Most common among people between 5-19 years.
• Particularly common in crowded conditions
(college dorms, military barracks).
– Mini epidemics in barracks, families, and
dormitories

12. • Clinical features:
– Headache, fever, chills, nausea ,vomiting and
photophobia.
– Joint symptoms (pain) and skin rash also
common.
– All close contacts to receive rifampicin.
• Morphology
– Brain: exudate over the surface and within
the leptomeninges.
– Acute inflammation accompanied by
neutrophilic infiltrate  purulent meningitis.
– CSF: cloudy or purulent
• Gram stain: diplococci within neutrophils

13. Brain: purulent exudate
over the surface

14. Neutrophilic infiltrate
in meningesPurulent CSF

15. Gram negative diplococci within a
neutrophil

16. Neisseriae gonorrhea
• Also know as gonococcus.
• Gram negative Intracellular diplococcous.
• Unencapsulated (unlike meningococcous)
• Causative agent of gonorrhea.
– Second most common STD
– Sexually transmitted infection of
epithelium
• Manifests as urethritis, cervicitis,
proctitis and conjunctivitis.

17. • Most frequently reported infectious disease in
the US.
• Transmission:
– Sexual contact
– Passage through birth canal.
– Women more likely to be asymptomatic
carriers than men
– Men more likely to transmit the disease than
women after each sexual exposure
• Virulence factors
• Pili: hair like surface appendages
– Enhance attachment.
– Confer resistance to phagocytosis.

18. Gonorrhea
• In males, the primary site
of infection is the urethra
– Purulent urethral
discharge
– Dysuria
• 95% of men have symptoms
• Complications =
epididymitis, prostatitis and
uretheral strictures

19. Neisseria gonorrhea urethritis

20. Gonorrhea (cont.)
• In women, the primary site of
infection is the cervix
(endocervical columnar
epithelial cells)
– Vaginal discharge
– Dysuria (b/c of urethritis
just like males)
– Abdominal pain
• Complications:
• Ascending genital infection:
– Salpingitis, endometritis,
oophoritis and tuboovarian
abscess = PID

21. • PID complications:
– Infertility 
tubal scarring
– Ectopic pregnancy
– Perihepatitis:
(Fitz-Hugh-Curtis
syndrome)
• Inflammation
of liver capsule
Tubo-ovarian mass

22. Other Gonococcal Diseases
• Rectal infections: male homosexuals
– Constipation, painful defecation with purulent
discharge.
• Pharyngitis:
– Oral genital contact
– Purulent exudate.
• Disseminated infections:
– Septic arthritis: most common cause of
arthritis in sexually active males.
– Septic arthritis involves the knees, wrists or
ankle joints.
– Tenosynovitis: wrists, fingers, ankles.

23. Other Gonococcal Diseases
• Purulent conjunctivitis in
newborns = Ophthalmia
neonatorum:
• Infection acquired during
delivery
• Inflammation of conjunctiva
and cornea  blindness
• This is why all newborns get
gentamicin drops in their
eyes. (Used to be silver
nitrate)
• D/D Chlamydia trachomatis

24. Diagnosis
• Gram Stain:
– Urethral exudate
 men
– ? Endocervical
smear  women
• Culture:
– Thayer-Martin
medium

25. Case 2
• CC
– A 2-year-old female is brought to the
emergency room because of paroxysms of
multiple coughs in a single expiration,
followed by a high-pitched inspiratory
whistle or whoop.
• HPI
– For the past two weeks she has had a
runny nose, low-grade fever, muscle
pains, and headache. Her immunization
schedule is incomplete.

26. • PE
– Fever,child apprehensive and
becomes cyanotic during cough
paroxysm; thick green mucus
expelled with cough; conjunctival
injection.
• Labs:
– CBC: marked leukocytosis with
lymphocytosis.

27. Bordetella pertussis
Whooping cough

28. Bordetella pertussis
• Small, non-motile, gram negative
coccobacilli.
• Pertussis = violent cough
• Whooping cough:
– Highly communicable illness
– Characterized by:
• Paroxysms of violent coughing followed
by a loud inspiratory whoop.
• Most children are less than one year old

29. Whooping cough
• Three stages
• Catarrhal stage:
– Characterized by features of common cold
– Rhinorrhea, sneezing, low grade fever.
– Most contagious stage b/c of droplet nuclei
and production of many organisms
• Paroxysmal stage:
– Characterized by classic whooping cough
paroxysms.
– 15/25 attacks / day
– Lymphocytosis
• Convalescent stage :
– Less number of attacks
– patient no longer contagious

30. This child has pertussis. It is difficult
for him to stop coughing and to get air.

31. – Secondary complications
• Infections
–Otitis media
–Pneumonia due to impaired
clearing mechanisms
• Physical sequelae of paroxysms -
hemorrhages, cracked ribs and
rectal prolapse!

32. Whooping Cough
Pathogenesis
• Source = clinically ill patient or carrier
• Pathogenesis
– Organisms attach to ciliated epithelial
cells
• hemagglutinin
• adhesin
– Proliferate intracellularly (protected)
– Produce toxins

33. Pertussis toxin
• The major cause of pertussis
• deregulation of cAMP (increased amounts
made) and decreased action of inhibitory G
protein by ADP-ribosylation  increased
respiratory secretions  paroxysmal cough to
get rid of fluid
• T cell lymphocytosis
• inhibits many leukocyte functions, including
– Chemotaxis ,phagocytosis and ,respiratory
burst
• paralyzes the cilia

34. Morphology
• Laryngotracheobron
chitis:
• Peribronchial
lymphadenopathy.
• Peripheral
lymphocytosis

35. • An opportunistic, gram negative water loving
bacteria.
• Important cause of infections in patients with:
1. Cystic fibrosis .
2. Compromised Immune system :
• HIV,Organ transplants, Burn patients
,Neutropenia and in
3. Hospitalized patients
• Nosocomial infections
• Is a blood vessel invader  hemorrhagic
infarctions
Pseudomonas aeruginosa

36. Pulmonary infections
• PSEUDOMONAS PNEUMONIA
– Common in patients with cystic fibrosis,
neutropenia, chronic lung disease and
patients on respirators.

37. Skin infection
• Most commonly infection of burn wounds.
– May lead to bacteremia
– Very difficult to control – burned tissue is not
very vascular so no PMNs to control infection
• Folliculitis
– Usually acquired from hot tubs and swimming
pools with inadequate levels of chlorine
• Ecthyma gangrenosum : large, well demarcated
necrotic and hemorrhagic skin lesions seen
following bacteremia.

38. Pseudomonas folliculitis

39. Other infections
• Ear infections:
– External otitis : swimmer’s ear
– Malignant external otitis : invasive and
necrotizing infection involving bone ; seen in
Diabetics. Can lead to sepsis and death
• Endocarditis: assoc. with IV drug abusers
– Usually involves the tricuspid valve (like S.
aureus)
• CNS infections: meningitis and abscess
• Eye: keratitis and endophthalmitis (contact lens
users)
• Osteomyelitis: more common in
– Diabetics
– IVDA

40. Other infections
• UTI:
– In patients with
indwelling catheters.
– Pyelonephritis
• Bacteremia:
– Occurs in patients with
: neutropenia, burns,
DM, hematological
malignancies.
– Characteristic skin
lesion : Ecthyma
gangrenosum.

41. Yersinia pestis
Plague
• Acute febrile zoonotic disease
• Caused by infection with Yersinia
pestis.
• Gram negative intracellular bacterium.
• Rats (pests) harbor this organism.
• Transmitted by: flea bites or
aerosols.
• flea acquires organisms during blood
meal from infected rats.

42. Xenopsylla cheposis (rat flea)

43. Clinical syndromes
• The flea regurgitates before it
feeds; injects the organism into
the human or the rodent.
• Three clinical manifestations
are:
1. Bubonic plague
2. Pneumonic plague.
3. Septicemic plague

44. Bubonic plague
• Most common type of disease.
• Infected rat flea bites on the extremity and
inoculates the bacilli.
• Bacilli intercepted by regional lymphnodes
bacilli proliferate within macrophages
• Patients have high fever, and painful , enlarged
tender lymphnodes = BUBO. (inflammatory
swelling of the lymphnodes).
• The buboes become soft , pulpy and tender.
• May infarct or rupture through the skin.
• Bacteremia DIC, bleeding  shock  death
(75%).

45. Inguinal Buboes Buboes: axilla

46. Pneumonic plague
 occurs when the plague bacteria infect the
lungs.
 Highly infectious and most frequently
fatal.
 Transmission occurs via respiratory
droplets contaminated with plague
bacteria.
 Clinical features:
 Initially fever  pulmonary signs
hemorrhagic and necrotizing
bronchopneumonia with fibrinous
pleuritis.

47. Septicemic plague
 occurs when plague bacteria are present in
the blood and begin to multiply
 Results as a complication of bubonic or
pneumonic plague.
 Induces DIC with hemorrhage and thrombi
 shock
 Lymphnodes throughout the body develop
foci of necrosis
 Gangrenous necrosis  black death

48. Blood smear – Safety pin appearance of Y.pestis

49. Chancroid (soft chancre)
• A sexually transmitted disease caused by
the gram negative rod Hemophilus ducreyi.
• Characterized by :
– Multiple painful ulcer on the penis and
the vulva often associated with tender
and enlarged inguinal lymphnodes.

51. Epidemiology
• Transmission:
– almost exclusively by sexual contact.
• Prostitution:
– a major cause of spread (seen a lot
during Korean and Vietnam wars).
• One of the most common causes of
genital ulcers in Africa and Southeast
Asia.
• Incidence increasing in US

52. Pathology and pathogenesis
• The organism enters the body through skin
abrasions.
• 1-14 days after exposure  tender papule on
the genitalia  painful ulcer.
• The ulcer lacks induration and is referred to as
a soft chancre .
• In contrast to the syphilis chancre, the
chancroid is extremely painful.
• Base of ulcer covered with shaggy,yellow-gray
exudate
• Regional lymphadenopathy
• Initially the lesion is typically solitary but by
autoinoculation multiple lesions develop.

53. Microscopy :Ulcer
• Superficial zone of neutrophils and
fibrin
• Underlying layer of granulation tissue
• Lymphoplasmacytic infiltrate
• Gram stain of aspirate: classic school
of fish orientation of the bacteria.

54. Haemophilus ducreyi
• = Ducrey's
bacillus is a
Gram(-) rod
• forms chains &
parallel
aggregates
“school of fish”
•

55. Differential diagnosis
1. Primary genital herpes type 2
infection
2. Primary syphilis
3. Lymphogranuloma venereum
4. Granuloma inguinale
5. Trauma

56. Granuloma inguinale
• Chronic, progressively destructive bacterial
infection of the genital region.
• Caused by:
– Calymmatobacterium granulomatis (Donovan’s
bacillus)
• A gram negative coccobacillus closely related
to Klebsiella.
• The organism is sexually transmitted.
• Phagocytosed by macrophages and are known as
– DONOVAN BODIES.

57. Epidemiology
• Granuloma inguinale:
– A venereal disease that is sexually
transmitted but
– not very contagious.
• endemic in the tropics and very rare in the
U.S.; probably < 100 cases/year.
• Pathogenesis
• The organism gains entry by direct
inoculation through skin abrasions or mucous
membranes.
• Indurated papules form  ulcerate

58. Morphology
• Begins as papular lesion
– Genitalia
– Oral mucosa/ pharynx
• Undergoes ulceration and is accompanied by
Granulation tissue formation 
•  give rise to protuberant soft painless
mass.
• Healing may occur by Scarring
– Development of strictures  (urethra,
vulva, anus)
• Regional lymphnodes are spared (c/f
Chancroid)

60. Microscopy
• Reactive epithelial hyperplasia at the
border of ulcer (mimicking ca =
pseudoepitheliomatous hyperplasia)
• The most important diagnostic feature :
– Giemsa stain of exudate:
• minute encapsulated coccobacilli
(Donovan bodies) in macrophages.