12- Microbiology Explains Flashcards

(237 cards)

1
Q

Campylobacter
jejuni

A

Most common cause of acute infective diarrhoea
Spiral, gram negative rods
Usually infects caecum and terminal ileum. Local
lymphadenopathy is common
May mimic appendicitis as it has marked right iliac
fossa pain
Reactive arthritis is seen in 1-2% of cases

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2
Q

Shigella spp.

A

Members of the enterobacteriaceae
Gram negative bacilli
Clinically causes dysentery
Shigella soneii is the commonest infective organism
(mild illness)
Usually self limiting, ciprofloxacin may be required if
individual is in a high risk group

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3
Q

Salmonella spp

A

Facultatively anaerobic, gram negative,
enterobacteriaceae
Infective dose varies according to subtype
Salmonellosis: usually transmitted by infected meat
(especially poultry) and eggs

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4
Q

E. coli

A

Enteropathogenic
Enteroinvasive: dysentery, large bowel
necrosis/ulcers
Enterotoxigenic: small intestine, travelers diarrhoea
Enterohaemorrhagic: 0157, cause a haemorrhagic
colitis, haemolytic uraemic syndrome and thrombotic
thrombocytopaenic purpura

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5
Q

Yersinia
enterocolitica

A

Gram negative, coccobacilli
Typically produces a protracted terminal ileitis that
may mimic Crohns disease
Differential diagnosis acute appendicitis
May progress to septicaemia in susceptible
individuals
Usually sensitive to quinolone or tetracyclines

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6
Q

Vibrio cholera

A

Short, gram negative rods
Transmitted by contaminated water, seafood
Symptoms include sudden onset of effortless
vomiting and profuse watery diarrhoea
Correction of fluid and electrolyte losses are the
mainstay of treatment
Most cases will resolve, antibiotics are not generally
indicated

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7
Q

What is the mechanism of action for quinolones, metronidazole, sulphonamides, and trimethoprim?

A

Quinolones (e.g. ciprofloxacin), metronidazole, sulphonamides, and trimethoprim inhibit DNA synthesis.

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7
Q

What is the mechanism of action for penicillins and cephalosporins?

A

Penicillins and cephalosporins inhibit cell wall formation.

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8
Q

What is the mechanism of action for aminoglycosides, chloramphenicol, macrolides, tetracyclines, and fusidic acid?

A

Aminoglycosides cause misreading of mRNA, chloramphenicol, macrolides (e.g. erythromycin), tetracyclines, and fusidic acid inhibit protein synthesis.

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9
Q

What is the mechanism of action for rifampicin?

A

Rifampicin inhibits RNA synthesis.

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10
Q

How can humans become infected with Fasciola hepatica?

A

Humans can become infected with Fasciola hepatica as part of a plant or food trematode infection.

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10
Q

What is Fasciola hepatica commonly known as?

A

Fasciola hepatica is commonly known as the common liver fluke, a parasitic trematode.

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10
Q

What symptoms are associated with the acute phase of Fasciola hepatica infection?

A

During the acute phase, the immature worms penetrate the gut, leading to symptoms such as fever, nausea, swollen liver, skin rashes, and extreme abdominal pain.

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11
Q

What is the recommended treatment for Fasciola hepatica infection?

A

The recommended treatment for Fasciola hepatica infection is triclabendazole.
Some patients may need ERCP

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11
Q

What symptoms are associated with the chronic phase of Fasciola hepatica infection?

A

During the chronic phase, the mature worms reside in the bile duct and can cause symptoms such as intermittent pain, jaundice, and anemia.

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12
Q

How can Fasciola hepatica be diagnosed?

A

Fasciola hepatica can be diagnosed through either a stool sample or serology.

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13
Q

What are the common organisms causing surgical infections?

A

Staphylococcus aureus, Streptococcus pyogenes, Escherichia coli, Campylobacter jejuni, H Polry

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14
Q

What are the characteristics of Staphylococcus aureus?

A

Gram positive coccus, facultative anaerobe, catalase positive, causes haemolysis on blood agar plates

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15
Q

What are the potential complications caused by Staphylococcus aureus toxins?

A

Toxic shock syndrome (exotoxin) and gastroenteritis (enterotoxin)

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16
Q

What is the ideal treatment for Staphylococcus aureus?

A

Penicillin, although resistance through beta-lactamase production is common

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17
Q

What virulence factors does Streptococcus pyogenes release into the host?

A

Hyaluronidase, streptokinase, and pyogenic exotoxin A

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17
Q

What is the prevalence of penicillin sensitivity in Staphylococcus aureus isolates in the UK?

A

Less than 5%

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18
Q

What are the characteristics of Streptococcus pyogenes?

A

Gram positive, forms chain-like colonies, Lancefield Group A Streptococcus, produces beta haemolysis

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19
Q

What condition can be caused by Streptococcus pyogenes releasing pyogenic exotoxin A?

A

Scarlet fever

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20
Which antibiotics are effective against Streptococcus pyogenes?
Penicillin (first-line) and macrolides (alternative)
21
What are the characteristics of Escherichia coli?
Gram negative rod, facultative anaerobe, non-sporing
22
What are the potential complications of Enterotoxigenic E. coli infection?
Large volume fluid secretion into the gut lumen and diarrhea
23
What are the characteristics of Campylobacter jejuni?
Curved, gram negative, non-sporulating bacteria
24
What is one of the commonest causes of diarrhea worldwide?
Campylobacter jejuni
25
What is the recommended approach for treating Campylobacter jejuni infection?
Antibiotics are not usually advised, but quinolones are often effective
26
What are the characteristics of Helicobacter pylori?
Gram negative, helix shaped rod, microaerophillic, flagellated, and mobile
27
What does Helicobacter pylori produce that can derive energy from hydrogen released by intestinal bacteria?
Hydrogenase
28
What can Helicobacter pylori secrete that breaks down gastric urea?
Urease
29
How can Helicobacter pylori infection be diagnosed?
Serology or biopsy urease test during endoscopy
30
What is the approximate risk of peptic ulcer in patients colonized by Helicobacter pylori? What is the approximate risk of gastric cancer in patients colonized by Helicobacter pylori? What is the approximate risk of MALT lymphoma in patients colonized by Helicobacter pylori?
10-20% 1-2% Less than 1%
31
What is necrotizing fasciitis?
Advancing soft tissue infection associated with fascial necrosis
32
What type of flora is responsible for causing necrotizing fasciitis, and what pathogen is increasingly seen in these cases?
Polymicrobial flora (aerobic and anaerobic), and Methicillin-Resistant Staphylococcus aureus (MRSA) is seen more frequently
33
Which organism is the most common isolated pathogen in necrotizing fasciitis infections?
Streptococcus (15% of cases)
34
What is Meleney's gangrene?
A similar principle to necrotizing fasciitis, but the infection is more superficially located and often confined to the trunk
35
What is Fournier's gangrene?
Necrotizing fasciitis affecting the perineum
36
What are the clinical features of necrotizing fasciitis?
Fever, pain, cellulitis, edema, induration, numbness; late findings include purple/black skin discoloration, blistering, hemorrhagic bullae, crepitus, and dirty dishwater fluid discharge
36
What types of bacteria are commonly involved in Fournier's gangrene?
Polymicrobial infection with E. coli and Bacteroides acting synergistically
37
What is the cornerstone of management for necrotizing fasciitis?
Radical surgical debridement
38
What is the recommended wound care for necrotizing fasciitis?
Sterile dressing
39
What is the causative agent of venereal syphilis?
Treponema pallidum (a spirochete)
40
What other mode of transmission can lead to syphilis?
Congenital infection
41
What is the typical lesion seen in primary syphilis?
Chancre (an indurated papule that forms an ulcer)
42
How long does it take for the chancre to appear after infection?
10-90 days
43
How does the chancre typically feel and how does it mimic carcinoma?
Hard and painless; it can resemble a hard ulcer with enlarged regional lymph nodes
44
What are the histological appearances seen on biopsy of the chancre?
Non-specific dense inflammatory infiltrates
45
How can the diagnosis of syphilis be confirmed?
By demonstrating spirochetes from the chancre using dark ground illumination microscopy or through serological testing for anti-treponemal antibodies
46
When does secondary syphilis typically develop?
Around 6 weeks following exposure to the disease
47
What is a common manifestation of secondary syphilis?
Widespread roseolar eruption
48
What can happen after treatment of syphilis?
Jarisch-Herxheimer reaction, characterized by fever and malaise, due to the release of antigens as the organisms die
49
What can occur in individuals who are not treated for syphilis?
Development of tertiary syphilis, characterized by the formation of gummas or diffuse inflammatory lesions
50
Which part of the aorta does syphilis typically affect in tertiary syphilis?
Proximal aspect
51
What can result from syphilis affecting the aorta?
Atypical aneurysms
52
What percentage of healthcare-associated infections do SSI comprise?
Up to 20%
52
What can cause surgical site infections (SSI)?
Breach in tissue surfaces that allow normal commensals and other pathogens to initiate infection
52
What percentage of patients undergoing surgery will develop an SSI?
At least 5%
53
Where do the organisms causing SSI often come from?
The patient's own body
54
What are some measures that may increase the risk of SSI?
Shaving the wound with a razor (preferably use a disposable clipper), using a non-iodine impregnated incise drape, tissue hypoxia, delayed administration of prophylactic antibiotics in tourniquet surgery
55
When should body hair be removed prior to surgery?
It should not be removed routinely; if necessary, use electrical clippers with a single-use head (razors increase infection risk)
56
When should antibiotic prophylaxis be considered?
For placement of prosthesis or valve, clean-contaminated surgery, and contaminated surgery; use antibiotics from the local formulary and aim to give a single dose intravenous antibiotic during anesthesia
57
What should be used to prepare the skin before surgery for the lowest incidence of SSI?
Alcoholic chlorhexidine
58
What should be done to cover the surgical site during the procedure?
Apply a dressing
59
Does administration of supplementary oxygen reduce the risk of wound infection?
No, recent meta-analysis has confirmed that it does not reduce the risk of wound infection
60
Do wound edge protectors confer benefit in preventing SSI?
No, they do not appear to confer benefit
61
What tissue viability advice should be followed for management of surgical wounds healing by secondary intention?
Follow tissue viability advice
62
Is the use of diathermy for skin incisions advocated in the NICE guidelines?
No, it is not advocated
63
Has the use of diathermy for skin incisions been shown to increase the risk of SSI?
No, several randomized controlled trials have demonstrated no increase in risk of SSI when diathermy is used
64
What organism causes enterobiasis?
Enterobius vermicularis
64
What is the common symptom of enterobiasis?
Pruritus ani (itching around the anus)
65
How is the diagnosis of enterobiasis usually made?
By placing scotch tape at the anus to trap eggs for microscopic examination
66
What are the common symptoms of Ancylostoma duodenale infection?
Most infections are asymptomatic, but it can cause iron deficiency anemia
66
What is the treatment for enterobiasis?
Mebendazole
67
How can Ancylostoma duodenale infection be diagnosed?
Larvae may be found in stools left at ambient temperature; otherwise, infection is difficult to diagnose
68
What is the treatment for Ancylostoma duodenale infection?
Mebendazole
69
How does Ancylostoma duodenale infection occur?
Infection occurs through cutaneous penetration, migration to lungs, being coughed up, and then swallowed
70
Which parasite causes Ascariasis?
Ascaris lumbricoides (roundworm)
71
How does Ascariasis infection occur?
Infections begin in the gut following ingestion, then the worms penetrate the duodenal wall to migrate to the lungs, are coughed up, and then swallowed
72
How is the diagnosis of Ascariasis made?
By identifying worms or eggs in the feces
73
What is the treatment for Ascariasis?
Mebendazole
74
Which parasite causes Strongyloidiasis?
Strongyloides stercoralis
75
How does Strongyloidiasis infection occur?
Initial infection is via skin penetration, then migration to the lungs, being coughed up and swallowed; mature worms in the small bowel are excreted, and the cycle begins again
76
What are the symptoms of Strongyloidiasis?
Individuals may be asymptomatic, but can also have respiratory disease and skin lesions
77
What is the autoinfective cycle recognized in Strongyloidiasis?
Larvae penetrating the colonic wall
78
How is the diagnosis of Strongyloidiasis usually made?
By stool microscopy
79
What is the treatment for Strongyloidiasis in the UK?
Mebendazole
80
What is the causative organism of Cryptosporidium infection?
Cryptosporidium (a protozoan)
81
How is Cryptosporidium infection transmitted?
Through the excretion of cysts, causing new infections
82
What are the symptoms of Cryptosporidium infection?
Diarrhea and cramping abdominal pains, which are worse in immunosuppressed people
83
How can Cryptosporidium infection be diagnosed?
Identification of cysts in stools
84
What is the treatment for Cryptosporidium infection?
Metronidazole
85
Which parasite causes Giardiasis?
Giardia lamblia (protozoan)
86
How does Giardiasis infection occur?
Through the ingestion of cysts
87
What are the symptoms of Giardiasis?
Gastrointestinal symptoms such as abdominal pain, bloating, and passage of soft or loose stools
88
What are the typical liver function test patterns for hepatic jaundice?
High bilirubin levels, elevated ALT/AST levels, elevated alkaline phosphatase levels (often very high)
89
How is the diagnosis of Giardiasis made?
By serology or stool microscopy
90
What are the typical liver function test patterns for post hepatic jaundice?
High to very high bilirubin levels, moderate elevation of ALT/AST levels, high to very high alkaline phosphatase levels
90
What is the first-line treatment for Giardiasis?
Metronidazole
91
What are the typical liver function test patterns for pre hepatic jaundice?
Normal or high bilirubin levels, normal ALT/AST levels, normal alkaline phosphatase levels
92
What is a specific feature of post hepatic jaundice that should be addressed in the history?
Pale-colored stools
93
What are the typical features and pathogenesis of gallstones?
Typical features: history of biliary colic or cholecystitis; Pathogenesis: small calibre gallstones that can pass through the cystic duct or stone compression of the bile duct in Mirizzi syndrome
94
What are the typical features and pathogenesis of cholangitis?
Typical features: obstructive symptoms (pain, fever, jaundice); Pathogenesis: ascending infection of the bile ducts, usually by E. coli, occurring in stagnant bile
95
What are the typical features and pathogenesis of pancreatic cancer?
Typical features: painless jaundice with palpable gallbladder (Courvoisier's Law); Pathogenesis: direct occlusion of distal bile duct or pancreatic duct by tumor
96
What are the typical features and pathogenesis of cholangiocarcinoma?
Typical features: gradual onset of obstructive pattern jaundice; Pathogenesis: direct occlusion by disease and extrinsic compression by nodal disease at the porta hepatis
97
What are the typical features and pathogenesis of TPN-associated jaundice?
Typical features: painless jaundice with non-obstructive features; Pathogenesis: hepatic dysfunction and fatty liver due to long-term TPN usage
98
What are the typical features and pathogenesis of bile duct injury?
Typical features: sudden or gradual onset of obstructive-type jaundice; Pathogenesis: injury during difficult cholecystectomy, leading to bile duct excision or stenosis caused by clips or diathermy
99
What are the typical features and pathogenesis of septic surgical patient?
Typical features: hepatic features; Pathogenesis: combination of impaired biliary excretion and drugs such as ciprofloxacin causing cholestasis
100
What are the typical features and pathogenesis of metastatic disease?
Typical features: mixed hepatic and post hepatic jaundice; Pathogenesis: combination of liver synthetic failure (late) and extrinsic compression by nodal disease and anatomical compression of intrahepatic structures (earlier)
101
What is the most commonly used first-line test for diagnosing liver and biliary conditions?
Ultrasound of the liver and biliary tree
102
What information does an ultrasound provide in diagnosing liver and biliary conditions?
Bile duct calibre, presence of gallstones, visualization of pancreatic masses and other lesions
103
What test should be performed if pancreatic neoplasia is suspected?
Pancreatic protocol CT scan
104
What test is often preferred for liver tumors and cholangiocarcinoma?
MRI or MRCP
105
What imaging technique may be used to stage certain malignancies but is not routinely part of first-line testing?
PET scan
106
What is the next step if MRCP fails to provide adequate information?
ERCP (Endoscopic Retrograde Cholangiopancreatography)
107
What should be addressed in the management of jaundice?
Relief of jaundice, screening and addressing clotting irregularities
108
What is the treatment approach for patients with malignancy causing jaundice?
Insertion of a stent (metal or plastic)
109
What surgical intervention is required for patients with a bile duct injury?
Repair of the defect or hepatico-jejunostomy if the bile duct has been excised
110
What alternative strategy can be used if stenting fails in patients with bile duct/pancreatic head malignancy?
Percutaneous drainage of the biliary system via a transhepatic route
111
How can gallstones be treated?
ERCP for stone removal and cholecystectomy
112
What should be done for patients with cholangitis?
High-dose broad-spectrum antibiotics, followed by biliary decompression
113
What are oncoviruses?
Viruses that cause cancer
114
How can oncoviruses be detected? How can oncoviruses be prevented?
Through blood tests By vaccines
115
Which virus is associated with Burkitt's lymphoma, Hodgkin's lymphoma, post-transplant lymphoma, and nasopharyngeal carcinoma?
Epstein-Barr virus
116
Which virus is associated with cervical cancer, anal cancer, penile cancer, vulval cancer, and oropharyngeal cancer?
Human papillomavirus
117
Which virus is associated with Kaposi's sarcoma?
Human herpes virus 8
118
Which virus is associated with hepatocellular carcinoma?
Hepatitis B virus and Hepatitis C virus
119
Which virus is associated with tropical spastic paraparesis and adult T cell leukemia?
Human T-lymphotropic virus 1
120
What is the most common benign tumor of mesenchymal origin in the liver?
Haemangioma
121
What is the incidence of haemangiomas in autopsy series?
8%
122
How do haemangiomas appear clinically?
Reddish purple hypervascular lesions
123
How are haemangiomas typically separated from normal liver tissue?
By a ring of fibrous tissue
124
What are the ultrasound characteristics of haemangiomas?
Hyperechoic
125
What is the demographic most commonly affected by liver cell adenomas?
Women in their third to fifth decade
126
What is the link between liver cell adenomas and the use of oral contraceptive pills?
They are linked to the use of oral contraceptive pills
127
How do liver cell adenomas appear on ultrasound and CT scans?
Mixed echoity and heterogeneous texture on ultrasound, hypodense on CT (prior to contrast administration)
128
When may removal of liver cell adenomas be required?
In patients with hemorrhage or symptoms
129
What are mesenchymal hamartomas?
Congenital and benign liver lesions usually present in infants
130
What is a major predisposing factor for liver abscesses?
Biliary sepsis
131
What are common symptoms of liver abscesses?
Fever, right upper quadrant pain, jaundice (in 50% of cases)
132
Where do the majority of amoebic liver abscesses occur?
In the right lobe of the liver
132
What is the most common extra-intestinal manifestation of amoebiasis?
Liver abscess
133
What are the typical presenting complaints of amoebic liver abscesses?
Fever and right upper quadrant pain
134
What do ultrasonography findings show for amoebic liver abscesses?
Fluid-filled structure with poorly defined boundaries
135
What is the treatment for amoebic liver abscesses?
Metronidazole
136
What causes hydatid cysts in the liver?
Echinococcus infection
137
What is the typical presentation of hydatid cysts?
Malaise and right upper quadrant pain
138
What are the ultrasound characteristics of hydatid cysts?
Unilocular cysts, thick cyst wall, external laminated hilar membrane, internal enucleated germinal layer, septa, and hydatid sand or daughter cysts
139
What is the treatment for hydatid cysts?
Sterilization with mebendazole followed by surgical resection
140
What is the association between polycystic liver disease and polycystic kidney disease?
Usually occurs together
141
What is the inheritance pattern of polycystic liver disease?
Autosomal dominant
142
What can cause symptoms in polycystic liver disease?
Capsular stretch
143
What are the characteristics of cystadenomas?
Rare lesions with malignant potential, usually solitary multiloculated lesions
144
What are the ultrasound characteristics of cystadenomas?
Large anechoic, fluid-filled area with irregular margins, internal echoes from septa
145
What is the recommended treatment for cystadenomas?
Surgical resection
146
How is Hepatitis B primarily transmitted?
Exposure to infected blood or body fluids
147
What is the incubation period of Hepatitis B?
6-20 weeks
148
How many doses of the hepatitis B vaccine are usually given, and when is a booster recommended?
3 doses, with a one-off booster 5 years following the initial primary vaccination
149
What is the composition of the hepatitis B vaccine?
HBsAg absorbed onto aluminium hydroxide adjuvant, prepared from yeast cells using recombinant DNA technology
150
Who are the at-risk groups that should be vaccinated against hepatitis B?
Healthcare workers, intravenous drug users, sex workers, close family contacts of individuals with hepatitis B, individuals receiving regular blood transfusions, chronic kidney disease patients nearing renal replacement therapy, prisoners, and chronic liver disease patients
151
What percentage of adults may fail to respond or respond poorly to the hepatitis B vaccine?
Around 10-15%
152
What are some risk factors for poor response to the hepatitis B vaccine?
Age over 40 years, obesity, smoking, alcohol excess, and immunosuppression
153
When is testing for anti-HBs recommended?
For those at risk of occupational exposure (e.g., healthcare workers) and patients with chronic kidney disease, with levels checked 1-4 months after primary immunisation
154
What are some complications of hepatitis B infection?
Chronic hepatitis, fulminant liver failure, hepatocellular carcinoma, glomerulonephritis, polyarteritis nodosa, cryoglobulinemia
155
What was the traditional treatment for hepatitis B, and what is its response rate?
Pegylated interferon-alpha, with up to 30% reduction in viral replication in chronic carriers
156
What are some predictors of a better response to pegylated interferon treatment?
Being female, < 50 years old, low HBV DNA levels, non-Asian, HIV negative, high degree of inflammation on liver biopsy
157
What is the current approach to treating hepatitis B with medication?
Oral antiviral medication to suppress viral replication, such as lamivudine, tenofovir, and entecavir
158
What does an anti-HBs level greater than 100 mIU/ml indicate?
Adequate response, no further testing required. A booster should still be received at 5 years.
159
What does an anti-HBs level less than 10 mIU/ml indicate?
Non-responder. Test for current or past infection. Give another vaccine course (3 doses) with testing following. If still no response, HBIG (Hepatitis B immune globulin) may be required for protection if exposed to the virus.
159
What does an anti-HBs level between 10 and 100 mIU/ml indicate?
Suboptimal response. One additional vaccine dose should be given. If immunocompetent, no further testing is required.
160
What is the most important alpha haemolytic streptococcus?
Streptococcus pneumoniae (pneumococcus)
161
What are the common clinical manifestations caused by Streptococcus pneumoniae?
Pneumonia, meningitis, and otitis media
162
Can you provide an example of another alpha haemolytic streptococcus?
Streptococcus viridans
163
How can beta haemolytic streptococci be further subdivided?
Group A and Group B
164
Which organism is the most important in Group A beta haemolytic streptococci?
Streptococcus pyogenes
165
What are some potential immunological reactions associated with Group A streptococcal infections?
Rheumatic fever and post-streptococcal glomerulonephritis
165
What causes scarlet fever in Group A streptococcal infections?
Erythrogenic toxins
166
What are some clinical conditions caused by Streptococcus pyogenes?
Erysipelas, impetigo, cellulitis, type 2 necrotizing fasciitis, and pharyngitis/tonsillitis
167
How is diarrhoea defined by the World Health Organisation? How long does acute diarrhoea typically last? How long does chronic diarrhoea persist for?
More than 3 loose or watery stools per day Less than 14 days More than 14 days
167
Which organism in Group B beta haemolytic streptococci can lead to neonatal meningitis and septicaemia?
Streptococcus agalactiae
168
What are some diagnostic methods for diarrhoea?
Stool culture, abdominal and digital rectal examination
169
When should colonoscopy be considered in the diagnosis of diarrhoea?
When radiological studies are unhelpful
170
What additional tests may be considered in the diagnosis of diarrhoea?
Thyroid function tests, serum calcium, anti-endomysial antibodies, and glucose
171
What is the most common organism causing septic arthritis overall?
Staphylococcus aureus
172
Which organism should be considered in young adults who are sexually active?
Neisseria gonorrhoeae
173
What should be done before starting treatment for septic arthritis?
Obtain synovial fluid for analysis
174
What type of antibiotics should be used for septic arthritis?
Intravenous antibiotics that cover Gram-positive cocci
175
What are the recommended antibiotics for septic arthritis according to the BNF?
Flucloxacillin or clindamycin (if allergic to penicillin)
176
How long is the usual duration of antibiotic treatment for septic arthritis?
Several weeks (BNF states 6-12 weeks)
177
When might arthroscopic lavage be required in septic arthritis?
In some cases, arthroscopic lavage may be necessary
178
What procedure should be used to decompress the joint in septic arthritis?
Needle aspiration
179
What is osteomyelitis?
Osteomyelitis is an infection of the bone.
180
What are the common causes of osteomyelitis?
The common causes of osteomyelitis include Staphylococcus aureus, occasionally Enterobacter or Streptococcus species. In individuals with sickle cell disease, Salmonella species are also known to cause osteomyelitis.
181
What are the clinical features of osteomyelitis?
The clinical features of osteomyelitis include erythema (redness), pain, and fever.
182
What investigations are conducted for osteomyelitis?
For the diagnosis of osteomyelitis, X-ray imaging may show a lytic center with a ring of sclerosis. A bone biopsy and culture are also performed.
183
What is the treatment for osteomyelitis?
The treatment for osteomyelitis involves prolonged antibiotic therapy. In some cases, surgical removal of sequestra (necrotic bone) may be necessary.
184
What is acute tonsillitis?
Acute tonsillitis is a condition characterized by pharyngitis (inflammation of the throat), fever, malaise, and lymphadenopathy (enlarged lymph nodes).
185
What is the most common bacterial organism causing acute tonsillitis?
The most common bacterial organism causing acute tonsillitis is Streptococcus pyogenes.
186
What are the typical characteristics of the tonsils in acute tonsillitis?
In acute tonsillitis, the tonsils are typically swollen (oedematous), and yellow or white pustules may be present.
187
What condition can mimic acute tonsillitis?
Infectious mononucleosis can mimic the symptoms of acute tonsillitis.
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What is the recommended treatment for bacterial tonsillitis?
Bacterial tonsillitis is usually treated with penicillin-type antibiotics.
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What complication can occur in bacterial tonsillitis?
Bacterial tonsillitis can sometimes lead to the formation of a local abscess known as quinsy.
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What are the common symptoms of HIV seroconversion?
HIV seroconversion is symptomatic in 60-80% of patients and typically presents as a glandular fever type illness. The features include sore throat, lymphadenopathy, malaise, myalgia, arthralgia, diarrhea, maculopapular rash, mouth ulcers, and rarely meningoencephalitis.
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When does HIV seroconversion typically occur after infection?
HIV seroconversion typically occurs 3-12 weeks after infection.
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What tests can be used to diagnose HIV?
For diagnosis, antibodies to HIV may not be present initially. HIV PCR (polymerase chain reaction) and p24 antigen tests can confirm the diagnosis.
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What is the most common and accurate test for HIV?
The most common and accurate test for HIV is the HIV antibody test. It usually consists of both a screening ELISA (Enzyme Linked Immuno-Sorbent Assay) test and a confirmatory Western Blot Assay.
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When do most people develop antibodies to HIV?
Most people develop antibodies to HIV at 4-6 weeks, but 99% develop them by 3 months.
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What is the p24 antigen test used for?
The p24 antigen test is usually positive from about 1 week to 3-4 weeks after infection with HIV. It is sometimes used as an additional screening test in blood banks.
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What is cholangitis?
Cholangitis is a condition characterized by a combination of bacterial infection and biliary obstruction.
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What are the clinical features of cholangitis?
The clinical features of cholangitis include Charcot's triad, which consists of fever (present in 90% of cases), right upper quadrant pain, and jaundice. In severe cases, Reynolds pentad may be present, which includes the symptoms of Charcot's triad plus confusion and hypotension.
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What are the most common organisms that cause cholangitis?
The most common organisms that cause cholangitis, listed from most frequent to least frequent, are Escherichia coli, Klebsiella species, Enterococcus species, and Streptococcus species.
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What are the recommended investigations for diagnosing cholangitis?
The recommended investigations for diagnosing cholangitis are an ultrasound scan (USS) as the first-line test and a CT scan. In cases with high clinical suspicion and suitability for treatment, endoscopic retrograde cholangiopancreatography (ERCP) may be performed as the first-line investigation.
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What does MRSA stand for?
MRSA stands for Methicillin-resistant Staphylococcus aureus.
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What is the treatment for cholangitis?
The treatment for cholangitis typically involves performing ERCP after 72 hours of antibiotic therapy. Another treatment option is percutaneous transhepatic cholangiogram and biliary drain.
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Who should be screened for MRSA?
In general, all patients awaiting elective admissions should be screened for MRSA. However, there are exceptions such as day patients having terminations of pregnancy and ophthalmic surgery. Patients admitted to mental health trusts are also excluded. In the UK, all emergency admissions are currently screened.
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Why is MRSA significant in the context of hospital-acquired infections?
MRSA was one of the first organisms that highlighted the dangers of hospital-acquired infections.
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What is the procedure for screening a patient for MRSA?
To screen a patient for MRSA, a nasal swab should be taken, and any skin lesions or wounds should also be swabbed. The swab should be wiped around the inside rim of a patient's nose for 5 seconds, and the microbiology form must be labeled as 'MRSA screen'.
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How can MRSA be suppressed in carriers once identified?
To suppress MRSA in carriers, mupirocin 2% in white soft paraffin should be applied to the nose three times a day for 5 days. Chlorhexidine gluconate should be applied to the skin once a day for 5 days, focusing on areas such as the axilla, groin, and perineum.
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Which antibiotics are commonly used in the treatment of MRSA infections?
vancomycin and teicoplanin.
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What is Salmonella?
Salmonella is a group of bacteria that includes many members, most of which cause diarrheal diseases. They are facultative anaerobes, Gram-negative rods that are not normally present as commensals in the gut.
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What are the common symptoms of typhoid and paratyphoid?
Typhoid and paratyphoid, also known as enteric fevers, typically present with systemic symptoms such as headache, fever, and arthralgia.
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Which specific types of Salmonella cause typhoid and paratyphoid?
Typhoid is caused by Salmonella typhi, while paratyphoid is caused by Salmonella paratyphi (types A, B, and C).
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Are there any other antibiotics that may be effective against MRSA?
Some strains of MRSA may be sensitive to antibiotics such as rifampicin, macrolides, tetracyclines, aminoglycosides, and clindamycin. However, these antibiotics should not generally be used alone because resistance may develop. Relatively new antibiotics such as linezolid, quinupristin/dalfopristin combinations, and tigecycline have activity against MRSA but should be reserved for resistant cases.
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What are the features of typhoid and paratyphoid?
The features of typhoid and paratyphoid include initially systemic upset as mentioned above, relative bradycardia (lower heart rate than expected), abdominal pain and distension, and constipation (which is more common in typhoid despite Salmonella being a recognized cause of diarrhea). In paratyphoid, rose spots may be present on the trunk in 40% of patients.
206
What are some possible complications of Salmonella infections?
Possible complications of Salmonella infections include osteomyelitis (especially in sickle cell disease, where Salmonella is one of the most common pathogens), gastrointestinal bleed or perforation, meningitis, cholecystitis, and chronic carriage, which occurs in approximately 1% of cases and is more likely in adult females.
207
What is mastitis?
Mastitis refers to an infection within the breast. The most common variant is lactational mastitis, which is related to breastfeeding. It occurs when the breast tissue, which may have breaks in epithelial integrity, becomes inoculated with Staphylococcus aureus carried in the infant's oropharynx. This results in a tender and erythematous breast. Fever is also common.
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How is mastitis typically treated?
The treatment for mastitis usually involves encouraging breast drainage, such as using breast pumps, along with the administration of antibiotics. Imaging with ultrasound (USS) can be used to identify any underlying abscess. Percutaneous aspiration is the preferred treatment for abscesses, if possible. In cases where the overlying epithelium is non-viable, debridement may be necessary. However, there is a risk of developing a subsequent mammary duct fistula as a complication.
209
What is a breast abscess?
A breast abscess is a collection of pus within the breast tissue. In lactating women, the most common cause of a breast abscess is Staphylococcus aureus infection.
210
What is malignant otitis externa?
Malignant otitis externa is an uncommon type of otitis externa that is primarily found in immunocompromised individuals, with approximately 90% of cases occurring in diabetics.
210
What are the typical symptoms of a breast abscess in lactating women?
In lactating women, a breast abscess typically presents as a tender and fluctuant (soft and compressible) mass in the breast.
210
How is a breast abscess diagnosed and treated?
The diagnosis of a breast abscess is usually made using ultrasound (USS) to visualize the abscess cavity. Treatment involves draining the abscess through a procedure, often guided by ultrasound. Antibiotics are also administered to treat the infection.
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What is the usual infective organism in malignant otitis externa?
Pseudomonas aeruginosa.
212
How does the infection progress in malignant otitis externa?
The infection starts in the soft tissues of the external auditory meatus (ear canal) and then progresses to involve the soft tissues and eventually the bony ear canal. In some cases, it can even progress to temporal bone osteomyelitis.
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What are some key features in the history of malignant otitis externa?
Key features in the history of malignant otitis externa include a history of diabetes (present in around 90% of cases) or immunosuppression due to illness or treatment. Patients may experience severe, unrelenting, deep-seated otalgia (ear pain), temporal headaches, purulent otorrhea (discharge from the ear), and possibly dysphagia (difficulty swallowing), hoarseness, and/or facial nerve dysfunction.
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What is the treatment for malignant otitis externa?
The treatment for malignant otitis externa typically involves the use of anti-pseudomonal antimicrobial agents, both systemic and topical. In some refractory cases, hyperbaric oxygen therapy may be used as an additional treatment.