Infectious Diseases Flashcards

1
Q

What is Cellulitis

A

It’s spreading inflammation of subcutaneous and fascial planes

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2
Q

Causative agents of Cellulitis

A

Streptococcus pyogenes and other Gram +ve bacteria.

Often Gram -ve bacteria like klebsiella, pseudomonas, E.coli.
Gram -ve causes secondary infections

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3
Q

Sequelae of cellulitis

A

Infection localised to form pyogenic abscess.
Infections to spread and cause bacteremia, septicemia, pyemia
Can also lead to local gangrene

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4
Q

Clinical features of Cellulitis

A

Fever, toxicity.
Swelling is diffused and spreading in nature
Cellulitis progresses rapidly in diabetic and immunosuppressed patients

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5
Q

Management of cellulitis

A

Elevation of limb or parts to reduce edema
Antibiotics
Dressing using glycerine to reduce edema because of hygroscopic action

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6
Q

Types of cellulitis

A

Orbital cellulitis
Ludwig’s Angina

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7
Q

Orbital cellulitis

A

It causes proptosis leading to impairment of ocular movements and blindness.
Can spread through ophthalmic veins into cavernous sinus causing cavernous sinus thrombosis.

Management through higher generation Antibiotics

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8
Q

What’s ludwig’s Angina

A

Cellulitis of upper part of neck involving submandibular region and floor of mouth along fascial planes

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9
Q

Clinical features of Ludwig’s Angina

A

Diffuse swelling, redness, tenderness, induration in floor of mouth and submandibular region.

Difficulty in mouth opening (trismus), dysphagia.
Fever, tachycardia and tachypnea.

Severe laryngeal edema.may require emergency tracheostomy.

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10
Q

Complications of Ludwig’s angina

A

Septicemia

Spread of infection into the parapharyngeal space leads to the thrombosis of the inter jugular vein which may extend above into sigmoid sinus which may be fatal

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11
Q

Treatment of Ludwig’s Angina

A

Antibiotics

Early surgical intervention under general anaesthesia.
Horizontal incision placed in submandibular region extending both side deepen to include deep fascia.
Myloid muscles are cut on both side to release tension, this prevents laryngeal edema and futher prevents spread of infection

When infection is controlled the incised wound is closed by secondary suture.
Occasionally loose sutures are placed with placement of drain into the wound

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12
Q

What is Erysipelas

A

It’s spreading inflammation of skin and subcutaneous tissues due to Streptococcus pyogenes.

There’s always cutaneous lymphangitis with rose pink rash and cutaneous lymphatic edema.

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13
Q

Sites of Erysipelas

A

Orbit
Face
Scrotum

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14
Q

Clinical features of Erysipelas

A

Toxemia
Rash is fast spreading
Discharge is serious
Milian’s ear sign

Common among individuals with poor hygiene

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15
Q

What is milian’s ear sign

A

A clinical sign.
Skin of ear mobile is adherent to subcutaneous tissue and so cellulitis cannot occur
Erysipelas being a cutaneous condition can spread into ear lobule

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16
Q

Treatment of Erysipelas

A

Penicillin
Amoxicillin
Cloxacillin

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17
Q

What’s pyogenic abscess

A

Localised collection of ous in a cavity lined by granulation tissue, covered by pyogenic membrane

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18
Q

Modes of infection of pyogenic abscess

A

Direct
Hematogenous
Lymphatics
Extension from adjacent tissues

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19
Q

Bacteria causing Pyogenic abscess

A

Staphylococcus aureus
Streptococcus pyogenes
Gram -ve bacteria
Anaerobes

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20
Q

Factors precipitating pyogenic abscess formation

A

General condition:- nutrition,age, anemia
Associated diseases:- diabetes, HIV, immunosuppressed patients
Types and virulence of organism
Trauma, hematoma, road traffic accidents

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21
Q

Clinical features of pyogenic abscess

A

Fever with chills and rigor
Localised swelling which is smooth, soft and fluctuant.
Visible pus
Throbbing pain and pointing tenderness
Brawny induration
Redness and warmth.

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22
Q

Site of pyogenic abscess

A

External:-
Finger and hands
Neck
Axilla
Breast
Foot, thigh
Ischiorectal and perianal
Abdominal wall
Dental abscess, tonsillar abscess

Internal:-
Abdominal
Perinephric
Retroperitoneal
Lung
Brain
Retropharyngeal

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23
Q

Investigations for abscess

A

Total count is raised.

Urine and blood sugar to rule out diabetes

Ultrasound sonography of abdomen and other region when required.

Xray in case of lung abscess

Gallium isotope

CT scan or MRI in case of brain and thoracic absess

Liver function test, PO2 and PCO2 tests, blood culture estimations

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24
Q

Complications of abscess

A

Bacteremia, Septicemia, pyemia
Multiple abscess formation
Destruction of tissues
Antibioma (common in breast abscess)
Large abscess may erode into adjacent vessels and can cause haemorrhage
Abscess in head and neck region can cause laryngeal edema, stridor and dysphagia.

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25
Q

Specific complications of internal abscess

A

Brain abscess can cause intracranial hypertension, epilepsy and neurological deficit.
Liver abscess can cause hepatic failure, rupture and jaundice.
Lung abscess can lead onto bronchopleural fistula or septicemia or respiratory failure or ARDS

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26
Q

Hilton’s method of draining abscess

A

Initially, broad spectrum antibiotics is started.
Under general anaesthesia or regional block anaesthesia, after cleansing and draping ,abscess is aspirated and presence of pus is confirmed .
Skin is incised in the line parallel to neurovascular bundle.
Pyogenic membrane is open using sinus forceps and all loculi are broken up.
Pus is cleared and washed away with saline.
A drain(guaze or corrugated rubber drain) is placed
Wound Is not closed and allowed to granulate and heal.
Sometimes secondary suturing or skin grafting is required.
Antibiotics are continued
Pus is sent for culture and sensitivity.

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27
Q

Problems in drainage of Abscess

A

Improper drainage
Bleeding
Residual abscess or sinus formation

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28
Q

Differential diagnosis of an abscess

A

Aneurysm, especially in femoral and popliteal and axillary region.
Aspirating with needle and confirming the pus is important.

Soft tissue tumors, Sarcomas maybe smooth and warmer

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29
Q

What is Boil

A

Also called Furuncle.
It’s an acute staphylococcal infection of hair follicle with perifolliculitis which proceeds to suppuration and Central necrosis

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30
Q

Treatment of boil

A

Antibiotics
Drainage of boil

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31
Q

Complications of boil

A

Cellulitis
Lymphadenitis
Hydradenitis (infection of a group of hair follicles)

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32
Q

Carbuncle

A

Word meaning is charcoal.
It’s an infective gangrene of skin and subcutaneous tissues

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33
Q

Main causative organism for carbuncle

A

Staphylococcus

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34
Q

Common site of carbuncle

A

Back and nape of neck

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35
Q

Carbuncle is common in

A

Diabetes and after 40 years of age .
In males
Patients will be toxic and in diabetic they will be ketotic

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36
Q

Investigations for carbuncle

A

Urine sugar and ketone bodies
Blood sugar
Discharge for culture and sensitivity

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37
Q

Treatment of carbuncle

A

Proper control of diabetes.
antibiotics
Drainage done by cruciate incision and debridement of all dead tissues.
Excision is done later

Once wounds granulate, skin grafting may be required

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38
Q

What’s Pott’s puffy tumor

A

Formation of diffuse external swelling in the scalp due to subperiosteal pus formation and scalp edema.
Originates in the frontal region and may extend into other

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39
Q

Causes of potts puffy tumor

A

Chronic frontal sinusitis.
Trauma causing frontal subperiosteal hematoma.
Chronic otitis nedia

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40
Q

Clinical features of potts puffy tumor

A

Pain and swelling in frontal region which is warm and tender
Toxicity and drowsiness

41
Q

Complications of potts puffy tumor

A

Osteomyelitis of frontal bone.
Spread of infection into the intracranial cavity leading to intracranial abscess.

42
Q

Investigations for Potts puffy tumor

A

Total leukocytes count
Erythrocytes sedimentation rate {ESR}
XRAY of skull
CT scan

43
Q

Differential diagnosis of Potts puffy tumor

A

Secondaries in brain or skull

44
Q

Treatment of Pott’s puffy tumor

A

Antibiotics and drainage under general anaesthesia before it spreads into cranial cavity.

Once it extends into cranial cavity, it’s treated by neurosurgical decompression using Dandy’s brain cannula.
Osteomyelitic brain often needs radical removal with proper reconstruction.

45
Q

Pyogenic granuloma

A

Common in face, scalp, fingers and toes.
Maybe due to minor trauma or minor infection.
Infection leads to unhealthy granulation tissue which protrudes through wound

46
Q

Clinical features of pyogenic granuloma

A

Single, well localised, red, firm, nodule which bleeds on touch.
May or May not be tender

47
Q

Sites for pyogenic granuloma

A

Face
Scalp
Fingers
Toes

48
Q

Differential diagnosis for pyogenic granuloma

A

Hemangioma
Papilloma
Skin adnexal tumours

49
Q

Treatment

A

Excision
Tissue sent for histopathological study

50
Q

Pyemia

A

Presence of multiplying bacteria in blood as emboli, spreads and lodge through different organs causing metastatic abscess.
Which may lead to multiple organ dysfunction syndrome.

51
Q

Clinical features of pyemia

A

Fever with chills and rigor
Jaundice, oliguria, drowsiness
Hypotension, peripheral circulatory collapse and later coma with MODS

52
Q

Common causes of Pyemia

A

Urinary infection
Biliary tract infection
Lower respiratory tract infection
Abdominal sepsis
Sepsis in diabetic and immunosuppressed individuals like HIV, steroids therapy

53
Q

Investigations for Pyemia

A

Total leukocytes count
Pus culture
Blood culture
Urine culture
Blood urea and serum creatinine
LFT

54
Q

Treatment of Pyemia

A

Monitoring of vital parameters
Antibiotics (ceftazidime, ceftoperazone, ceftriaxone sodium)
IV fluids, maintenance of urine output..
Hydrocortisone
Blood and plasma transfusion
Nasal oxygen, ventilator support, monitoring of pulmonary function

55
Q

What is Gonorrhea

A

Sexually transmitted disease caused by Niesseria Gonorrheae.
It’s a gram -ve Intracellular diplococcus.

56
Q

Where does gonorrhea affect and what’s its incubation period

A

It affects the epithelium of urogenital tract, rectum, pharynx, conjuntivae and anterior urethra (in male)

Incubation period:- 2-14 days

57
Q

Features of Gonorrhea

A

Dysuria and urethral discharge.
In females, vaginal discharge, dysuria, bilateral salpingitis and infertility.
After chronic infection,gonococcal urethritis causes urethral strictures usually in bulbar urethra.
It also causes epididymoorchitis, prostatitis and proctitis

58
Q

Diagnosis of Gonorrhea

A

Patient is asked to pass urine in two cups.
Haziness in first cup signifies infection with pus the second cup is clear.

Gram staining and culture of urine is diagnostic

59
Q

Treatment of Gonorrhea

A

Penicillin is DOC.
Ampicillin, ciprofloxacin, ceftriaxone , cefixime and spectinomycin are used.

In complicated Gonorrhea, prostatic massage, local irrigation, treatment for stricture urethra, Doxycycline and Gentamicin therapy are indicated.

60
Q

Acute pyomyositis

A

Infection and suppuration with destruction of skeletal muscles .

61
Q

Causative organism of acute pyomyositis

A

Staphylococcus aureus
Streptococcus pyogenes
And gram -ve bacteria

62
Q

Common site for acute pyomyositis

A

Thigh
Gluteal region
Shoulder and arm

63
Q

Clinical features for Acute pyomyositis

A

Creatine phosphokinase will be high and signifies acute phase.
Renal failure is common.

MRI is useful

64
Q

Treatment of acute pyomyositis

A

Antibiotics
Wound excision and compartment release often with hemodialysis.

65
Q

Anthrax

A

Caused by Bacillus anthracis which is gram +ve bacteria, spore forming, capsulated, non motile, non Acid fast bacillus.
Resistant to heat and antisepsis.

Common in cattle and seen in humans who handle carcasses,wool and hairs.

66
Q

Types of Anthrax

A

Cutaneous type-
common.
Occurs after 3-4 days after infection.
Indurated papular with black Slough and rounded by vesicles –malignant pustules.
Regional lymph nodes are involved.
Toxemia common.

Woolsorter’s disease is respiratory type. Due to inhalation of spores causing pneumonia.
More dangerous and life threatening.

Alimentary type- due to ingestion of spores

67
Q

Diagnosis of Anthrax

A

Culture shows Medusa head appearance.
Positive for M’Fadyean reaction and
Positive for Acoli’s thermoprecipitation test

68
Q

Treatment of Anthrax

A

Penicillins
Ciprofloxacin

69
Q

Tetanus

A

It’s an infective condition caused by clostridium tetani leading to relex muscle spasm often associated with tonic clinic seizures

70
Q

How is tenatus caused

A

Caused by clostridium tetani which is gram positive bacteria, anaerobic, mobile, non capsulated with petrichous flagella with terminal spores.

Spores are infective agent. Found in soil, manure, dust etc.

They gain entry into wound, prick injuries, accidents, foreign bodies, anaerobic conditions etc.

71
Q

Clinical features of tetanus:-
Symptoms

A

Jaw stiffness, pain and stiffness in neck and back muscles
Anxiousness and sweating
Headache, delirium, sleeplessness
Dysphagia
Dyspnea

72
Q

Clinical features of tetanus
Signs:-

A

Trismus, due to spasm of masseter and ptreygoids
Risus sardonicus (smiling face) due to spasm of zygomaticus major
Neck rigidity
Spasm and rigidity of all muscles
Hyperreflexia
Respiratory changes

73
Q

Which toxins are released in tetanus

A

Exotoxins:-
Tetanospasmin and tetanolysin.

74
Q

Tetanospasmin

A

Enters through the perineurial sheath into the CNS
BLocks Cholinesterase enzymes at anterior horn cells
Which causes hyperexcitability and reflex spasm of muscles with TONIC CLONIC CONVULSIONS

Once toxin is fixed in nerve tissue it can no longer be neutralized by antitoxin.

75
Q

Tetanospasmin another pathway

A

Circulation
Causes Toxemia through blood
Blocks the NMJ by acting on Cholinesterase
Aggrevates muscle spasm

76
Q

Tetanolysin

A

Causes hemolysin

77
Q

Pathogenesis of Tetanus

A

Tonic clonic convulsions
Abdominal wall rigidity and hematoma formation
Severe convulsions may often lead to fractures, joint dislocation and tendon ruptures.
Fever, Tachycardia
Retention of urine, constipation.
Rarely features of Carditis.
Symptoms will be aggrevated by stimuli like light, noise.

78
Q

Incubation period of tetanus

A

Time between entry of spore and appearance of first symptom.

7-10 days

79
Q

Period of Onset of Tetanus

A

Time between first symptom and first sign.

80
Q

Types of tetanus

A
  1. Early tetanus
  2. Latent tetanus
  3. Late tetanus
  4. Ascending tetanus
  5. Descending tetanus
  6. Cephalic tetanus
  7. Localised tetanus
  8. Bulbar tetanus
  9. Tetanus neonatorum
  10. Urban tetanus
81
Q

Different postures in tetanus

A
  1. Opisthotonus- backward bending.
  2. Orthotonus - straight posture
  3. Emprosthotonus - forward bending
  4. Pleurosthotonus- lateral bending.
82
Q

Staging of tetanus

A

Mildly I’ll - rigidity,spasm, trismus and different postures

Seriously ill- spasm, rigidity,severe respiratory infections

Dangerously ill- cyanosis with respiratory failure and tonic clonic convulsions

83
Q

Differential diagnosis of tetanus

A

Strychnine poisoning
Trismus due to dental oral, tonsillar sepsis, oral malignancy.
Meningitis
Hydrophobic
Convulsion disorders

84
Q

Treatment of Tetanus

A

Patient admitted in isolated, dark, quiet room.
Antitetanus globulin (ATG) 300 /units IM stat.
ATS when ATG is not available
After IV test dose (1000 units of ATS),full dose of ATS i.e, 1,00,000 units half by IM and half by IV is given
Wound debridement, drainage of pus, injection of ATG 250-500 units locally reduce toxin effect.
Ryle’s tube is passed to decompress and so as to prevent aspiration but later for feeding purpose.

Catheterization
IV fluids and electrolyte balance to be maintained
Tetanus toxoid to be given as disease will not give immunity against further infections

IV diazepam 20mg 4/6th hourly
IV phenobarbitone 30mg 6th hourly
IV chlorpromazine 25 mg 6th hourly
Injection crystallize penicillin 20lacs 6th hrly,
Inj. Gentamicin and metronidazole to prevent secondary infection.
Nasal oxygen
In severe cases, patient is curarised and placed in ventilators
Endotracheal intubation or tracheostomy are often life saving

Steroids to be given when Carditis is suspected

85
Q

Gas Gangrene in earlier days was called

A

Malignant Edema

86
Q

Organisms that cause Gas Gangrene

A

Clostridium purfringens. (welchii)
Clostridium oedematiens
Clostridium septicum
Clostridium histolyticus

87
Q

Which exotoxins are released in Gas Gangrene

A

Lecithinase (imp toxin- hemolytic, membranolytix and necrotic causing extensive myositis)
Hemolysin
Hyaluronidase (rapid spread of gas)
Proteinase

88
Q

Effects of Gas Gangrene

A

Extensive necrosis of muscle with production of H2S gas
Foaming liver- when it affects the liver causes necrosis with frothy blood.

89
Q

Incubation period of gas Gangrene

A

1-2 days

90
Q

Clinical features of Gas Gangrene

A

Toxemia, fever, tachycardia
Wound under tension with foul smelling discharge
Khaki coloured skin due to hemolysis.
Crepitus can be felt
Jaundice-maybe fatal

91
Q

Clinical types of Gas Gangrene

A

Fulminant type
Massive type
Group type
Single muscle type
Subcutaneous type

92
Q

Fulminant type of gas Gangrene

A

Causes rapid Progress and Often death
Due to Toxemia, renal failure of liver failure or MODS

93
Q

Massive type

A

Infection involving the whole of one limb containing fully dark coloured gas filled areas.

94
Q

Group type gas Gangrene

A

Involving one group of muscles

95
Q

Single muscle type of gas Gangrene

A

Affecting one single muscle

96
Q

Subcutaneous type of gas Gangrene

A

Involves only subcutaneous tissues

97
Q

Investigations for gas Gangrene

A

X ray shows gas in muscle plane or under the skin.
LFTs, blood urea, serum creatinine, total count, PO2, PCO2

98
Q

Treatment of gas Gangrene

A

Inj. Benzyl penicillin 20lacs 4th hourly +
Inj. Metronidazole 500mg 8th hourly +
Inj. Aminoglycoside (if blood urea is normal)

Fresh blood transfusion
Polyvalent antiserum 25000/unit after a test dose and repeat 6th hours.
Hyperbaric oxygen
Liberal incisions, all dead tissues and debridement is done until healthy tissues bleeds.
Rehydration and maintaining optimum urine output 30ml/hr.
Electrolyte management

In severe cases, amputation.

99
Q

Precautions after operating on a gas Gangrene patients in OR

A

They should be fumigated 24-48 hours properly to prevent risk of spread of infection to other patients.