anaerobic gram positive rods Flashcards

1
Q

name the sporing anaerobic gram positive rods

A

clostridium spp.: c. perfringens, c. tetani, c. septicum, c. botulinum, c. difficile

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2
Q

clostridium perfringens: character

A

frequently present in human faeces, may colonise the skin particularly below the waist, often causes outbreaks in geriatric wards

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3
Q

clostridium pefringens: culture

A

nagler plate test for alpha toxin; breaks down lipids of egg yolk in agar to produce insoluble fat droplets which is seen as an area of opacity

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4
Q

clostridium pefringens: virulence

A

alpha toxin (lecithinase): destroys cell membranes

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5
Q

clostridium perfringens: clinical presentations

A

gas gangrene (clostridial myonecrosis) occurs after spores are introduced into area of tissue which is anaerobic, resulting in rapid spreading tissue damage; gas is produced in this process (detected by pressing and feeling a crepitus or by x-rays)

local signs include pain, discolouration, fluid filled blebs and thin smely discharge; systemic illness also occurs, leading to shock and septicaemia

food poisoning: spores survive cooking, depths of food, presents with abdominal cramps and diarrhoea 12-24 hours after consumption

pigbel: necrotising enteritis in new guinea after eating pork feasts

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6
Q

clostridium perfringens: diagnosis

A

histology, culture, (blood, discharge, tissue)

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7
Q

clostridium perfringens: treatment

A

gas gangrene: benzylpenicillin + clindamycin (targets infetions involving toxins), removal of dead tissue
for food poisoning: rehydration therapy, anitibiotics are not indicated

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8
Q

clostridium septicum: clinical presentations

A

gas gangrene

isolation from the blood is associated with leukemia and colon cancer

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9
Q

clostridium difficile: character

A

found in faeces of a minority of the population

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10
Q

clostridium difficile: virulence factors

A

exotoxin

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11
Q

clostridium difficile: clinical presentations

A

antibiotics-associated pseudomembrane colitis
pseudomembrane formed in colon, usually precipitated by the use of antibiotics that wipe out normal gut flora

not all infections result in pmc, some cause a mild diarrhoeal disease

cdad: c. difficile associated diarrhoea

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12
Q

clostridium difficile: diagnosis

A

colonoscopy, stool culture, toxin detection (either through cytotoxicity or immuno-assays), pcr, gde antigen detection

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13
Q

clostridium difficile: treatment

A

stop antibiotics if possible, oral metronidazole or oral vancomycin; isolate patient + be wary of relapse

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14
Q

clostridium botulinum: character

A

direct wound ingection, ingestion of preformed toxin in contaminated food especially honey

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15
Q

clostridium botulinum: virulence factors

A

botulinum toxin blocks acetylcholine release at the neuromuscular junction

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16
Q

clostridium botulinum: clinical presentations

A

botulism - flaccid paralysis
early signs: diplopia, ptosis, nausea, vomitting, usually no fever
severe conditions: paralysis of respiratory muscles

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17
Q

clostridium botulinum: diagnosis

A

culture (patient sample or food), test for toxin by inoculation of mouse

18
Q

clostridium botulinum: treatment

A

antiserum to neutralise free toxin, mechanical ventilation

19
Q

clostridium tetani: histology + character

A

drumstick appearance (long thin rod with a large terminal spore)

found in faeces of large farm animals, human gut; soil; spores are widespread in environment

20
Q

clostridium tetani: virulence factors

A

tetanospasmin; a very potent neurotoxin which blocks inhibitory stimuli received by lower motor neurons

21
Q

clostridium tetani: clinical presentations

A

tetanus - spastic paralysis
local signs: pain and stiffness at site of infection
mild symptoms: lockjaw (masseter affected early); risus sardonicus
serious symtoms: opisthotonus (all muscles of back contract, body assumes rigid posture determined by the stronger of each antagonistic set of muscles), autonomic disturbance and eventually cvs derangements

*infection itself does not produce immunity to the toxin and immunisation is required

22
Q

clostridium tetani: treatment

A

human tetanus immunoglobulin (htig) to neutralise free toxin that is unbound to motor neurons
remove unhealthy tissue, prescribe antibiotics to kill remnant clostridia
paralysis and ventilation of patients with difficulty breathing due to spasms (wait until bound toxin is degraded); immunize after recovery since the infection is not immunogenicc

23
Q

clostridium tetani: prevention

A

toxoid vaccine in the national childhood immunisation schedule (beware of neonatal tetanus; every child has a wound that is the umbilicus)

24
Q

most non-sporing anaerobic gram positive and negative rods: antibiotics sensitivity

A

antibiotics sensitive:
metronidazole-sensitive
above umbilicus - penicillin sensitive, below unmbilicus: penicillin resistant (e.g. bacteroids fragilis that is part of the colonic flora produces beta lactamase)

25
Q

most non-sporing anaerobic gram positive and negative rods: nature of infections

A

often mixed, involving the aerobic species as well
seldom spontaneous, often involves precipitating cause (surgery, gut perforation, diabetes, cancer)
usually endogenous in nature (own flora), except for animal bites
produces disgusting smells

26
Q

most non-sporing anaerobic gram positive and negative rods: clinical presentations (head and neck)

A

vincent’s infection - acute necrotising ulcerative gingitvitis; painful ulcerations of the gums with bleeding, may spread to tonsils causing painful swallowing (vincent’s angina)
dental sepsis
abscess/cellulitis - submandibular infection leads to ludwig’s angina
chronic ent infection (sinusitis, otitis media, matoiditis)
brain abscess that involves streptococci too

treatment: metronidazole or penicillin (above umbilicus, hence susceptible)

27
Q

most non-sporing anaerobic gram positive and negative rods: clinical presentations (pleuropulmonary)

A

follows aspiration of mouth flora

pneumonia, lung abscess, empyema

28
Q

most non-sporing anaerobic gram positive and negative rods: clinical presentations (abdominal)

A

secondary to appendicitis, diverticulitis, abdominal surgery

peritonitis, abscess, wound infection, liver infection

  • diverticulitis: inflamed pouches in the GIT
    treatment: metronidazole or penicillin (above umbilicus, hence susceptible)
29
Q

most non-sporing anaerobic gram positive and negative rods: clinical presentations (skin and soft tissue)

A

infections of diabetic foot ulvers, decubitus ulvers, sebaceous cysts, hydradenitis suppuravita (infected blocked aprcrine glands)
acne (propionibacterium spp.)
anaerobic cellulitis (spreading infection of subcutaneous tissues, often involves clostridium spp and aerobic bacteria too)

30
Q

most non-sporing anaerobic gram positive and negative rods: clinical presentations (genital tracts)

A

male genital tract: scrotal and prostate infections

female genital tract:
bacterial baginosis
endometritis, tubo-ovarian sepsis, bartholin’s abscess, septic abortion, intrauterine devices associated infections, chronic pelvic inflammatory diseases
neonatal pneumonitis

treatment: metronidazole or clindamycin

31
Q

most non-sporing anaerobic gram positive and negative rods: clinical presentations (others)

A

urinary tract - very rare, often involves fistula connecting to bowel due to tumour invasion; suspected with foul smelling urine but no aerobic culture

bone and joint - uncommon cause of chronic osteomyelitis and septic arthritis

bacteraemia: commonly bacteroides fragilis (which has beta lactamase)

32
Q

synergistic infections between aerobic and anaerobic bacteria

A

necrotising fasciitis: s. pyogenes, anaerobes, clostridium spp., mrsa, vibrio vulnificus

meleney’s synergistic gangrene: spreading area of skin necrosis causing ulceration, usually starting at a post-operative abdominal wound site or colostomy; s. aureas + microaerophilic or anaerobic streptococci

fourneir’s gangrene: mixed infection of scrotum causing gangrene

33
Q

name the exceptions to the generalisation of non-sporing anaerobic gram positive and negative rods

A

actinomyces israelii

fusobacterium necrophorum

34
Q

actinomyces israelii: histology + character

A

gram positive branching filaments that are isolated from sulphur granules in pus

normal flora

35
Q

actinomyces israelii: clinical presentations

A

invasive infections following disease or trauma at mucosal surgaces, spreads slowly across tissue planes and causes fibrosis - hard swelling forms and eventually pus drains from sinus tracks onto skin surface

common sits: cervicofacial (commonst, predisposed by dental extraction and caries), thoracic (lung infection eventually invading chest well), abdominal (originates from diseased appendix or colon), pelvic (associated with use or intrauterine devices)

36
Q

actinomyces israelii: diagnosis

A

culture (slow-growing)

37
Q

actinomyces israelii: treatment

A

penicillin/amoxicillin, intravenous benzylpenicillin for serious disease

**resistant to metronidazole

38
Q

fusobacterium necrophorum: clinical presentation

A

gram negative
necrobacillosis - lemierre’s disease
severe sore throat, progressing to septicaemia which seeds bacteria to multiple organs, forms multiple abscesses
infection may locally invade the jugular vein and carotid artery

39
Q

fusobacterium necrophorum: diagnosis

A

culture (blood, abscess fluid)

40
Q

fusobacterium necrophorum: treatment

A

benzylpenicllin, drain abscesses