Infection Flashcards
(141 cards)
1
Q
What is the structure of adenovirus?
A
- Non-enveloped
- Icosahedral
- Double stranded linear DNA
2
Q
What respiratory diseases does adenovirus commonly cause?
A
- Acute febrile pharyngitis: Most common in infants and young children; characterised by a cough, sore throat, nasal congestion and fever.
- Pharyngoconjuctival fever: Conjunctivitis in addition to pharyngitis; occurs most commonly in school children and often within family groups or in groups using the same swimming facility.
- Acute respiratory disease: Occurs primarily in epidemics among new military recruits – thought to reflect the lowered resistance brought on by exposure to new strains, fatigue and crowded living conditions, promoting the efficient spread of the infection.
- Viral pneumonia: Progressions of the above conditions and has the mortality rate of 10% in infants.
3
Q
What gastrointestinal conditions does adenovirus cause?
A
Infantile gastroenteritis: Adenoviruses can multiply in the GI tract and can be found in stools. Two serotypes have been associated specifically with this disease. Adenovirus infections have been estimated to account for 5 to 15% of all viral diarrheal disease in children.
4
Q
What ocular conditions does adenovirus cause?
A
- Follicular conjunctivitis: Self-limiting and has no permanent sequelae.
- Keratoconjunctivitis: A more serious infection involving the corneal epithelium, which may be followed by corneal opacity lasting several years. Partly results from transmission via shared towels or ophthalmic solutions, person-to-person contact and improperly sterilised ophthalmological instruments.
5
Q
What are less common conditions caused by adenovirus?
A
- Haemorrhagic cystitis: Occurs primarily in boys and characterised by haematuria.
- Left ventricular dysfunction: Infection of the heart muscle in both children and adults.
- Pneumonia: Common in immunocompromised patients who contract a respiratory infection (e.g. patient with AIDS)
6
Q
What is the pathogenesis of adenovirus?
A
They are most commonly transmitted via the respiratory route. However, most adenoviruses also replicate efficiently and asymptomatically in the intestine and can be isolated from the stool well after the respiratory disease symptoms have ended, as well as from the stools of a healthy person. Similarly, ocular infections are transmitted by direct inoculation of the eye by virus-contaminated hands, ophthalmologic instruments or bodies of water in which groups of children swim together.
7
Q
What are laboratory tests for adenovirus?
A
Direct test of stool specimens by ELISA
8
Q
What are treatments and preventions against adenoviruses?
A
No antiviral agents are currently available. Prevention of the epidemic respiratory disease by immunisation has only been used for the protection of the military population. A vaccine containing live, unattenuated adenovirus types 4 and 7, formulated for oral administration has been licensed for use among the US military.
9
Q
Describe the structure of Clostridium difficile
A
Stain: Gram positive Shape: Bacillus Obligate Anaerobe Extra: Form spores, therefore making it very resistant to antibiotics Non-encapsulated but the spores are
10
Q
Name some antibiotics associated with clostridium difficile
A
- Ampicillin
- Cephalosporins
- Clindamycin
- Ciprofloxacin
- Amoxicillin
- Penicillins
- Sulphonamides
- Erythromycin
- Trimethoprim
- Quinolones
11
Q
Where can you normally find C.difficile in the body?
A
Clostridium difficile (C.diff) is a minor component of the normal flora of the large intestine.
12
Q
Why do use of some antibiotics increases the susceptibility to Clostridium difficile infections?
A
The antibiotics suppresses the more predominant C.diff in the large intestine so the number of invading C.diff increases as they have fewer organisms to compete with for attachment and resources.
13
Q
What is the pathogenesis of c.difficile?
A
C.diff produces 2 toxins; toxins A and B.
Toxin A is an enterotoxin that causes excessive fluid secretion but also stimulates an inflammatory response. Toxin B is a cytotoxin, which disrupts protein synthesis and causes disorganisation of the cytoskeleton. They are both glucosyltransferases.
14
Q
How is C.difficile found in the laboratory?
A
o ELISA to identify toxins A and B.
o PCR
o Cultured on blood agar
15
Q
What diseases can C.difficile cause?
A
o Pseudomembranous colitis
16
Q
What treatment do you use for C.difficile conditions?
A
o Oral metronidazole or vancomycin
17
Q
What is the structure of Clostridium perfringes?
A
Stain: Gram positive
Shape: Rod
Anaerobic
Encapsulated and produces endospore
18
Q
Where is clostridium perfringes seen as normal flora in the body?
A
GI tract and vagina
19
Q
What is the pathogenesis of C.perfringes?
A
o α Toxin – a lecithinase that degrades lecithin in mammalian cell membranes causing lysis of endothelial cells as well are erythrocytes, leukocytes and platelets.
o Enterotoxins act in the lower portion of the small intestine. LThe molecule binds to receptors on the epithelial cell surface and alters the cell membrane disrupting ion transport leading to loss of fluid and intracellular proteins.
o Produces a variety of hydrolytic enzymes.
20
Q
What are the laboratory findings for C.perfringes?
A
o Produces double zone of β haemolysis on blood agar
21
Q
What diseases do C.perfringes usually cause?
A
o Gas gangrene (myonecrosis) o Anaerobic cellulitis o Food poisoning o Necrotic enteritis o Clostridial endometritis
22
Q
What is the treatment for C.perfringes conditions?
A
o Penicillin G
o Clindamycin
o Metronidazole
23
Q
What is the structure of Escherichia Coli?
A
Stain: Gram negative Shape: Short rods Facultative Anaerobe Catalase positive Encapsulated
24
Q
What diseases does E.coli cause?
A
o UTI
o Neonatal meningitis
o Hospital acquired infections
25
What is the physiology of E.coli?
E. Coli can generate energy by aerobic or anaerobic respiration by using nitrate, nitrite or fumarate as terminal electron acceptors. There are many different serotypes.
26
What are laboratory findings of E.coli?
o Stool cultures
o Cultured on MacConkey agar
o Serology
o Isolation of E. Coli from normally sterile body sites is diagnostically significant
27
What is the treatment used for E.coli conditions?
UTI
o Ciprofloxacin/Trimethoprim
o Nitrofurantoin
```
Local or systemic disease
o Ampicillin
o Cefotaxime
o Ciprofloxacin
o Trimethoprim
```
Neonatal meningitis
o Cefotaxime
28
What is the structure of Haemophilus influenza?
Stain: Gram negative
Shape: Pleomorphic in shape ranging from small coccobacilli to long slender filaments – USUALLY RODS.
Anaerobic
Encapsulated
29
What are the diseases caused by H.infleunza?
◦Bacterial meningitis
◦Otitis media
◦Sinusitis
◦Pneumonia
◦Epiglottitis
◦Septic arthritis
30
Where is H.influenza usually found?
A normal component of the upper respiratory tract flora.
| Illnesses are usually sporadic in occurrence.
31
What is the pathogenesis of H.influenza?
H. influenzae is transmitted by respiratory droplets. Bacteria produce an IgA protease that cleaves IgA1 and thus evade the immunoglobulins of this class. It can also enter the bloodstream and disseminate to distant sites. Therefore diseases caused by this bacterium can be separated into two categories – contiguous spread e.g. otitis media and invasion of the bloodstream e.g. Septic arthritis.
32
How do you test for H.influenza in a laboratory?
Culture on chocolate agar with NAD+ and haemin.
33
What is the treatment for H.infleunza diseases?
◦Ampicillin
◦Cefotaxime
◦Ceftriaxone
◦Trimethoprim
34
What is the structure of helicobacter pylori?
Stain: Gram negative
Shape: Rod
Microaerophilic
Multiple polar flagella, which give organism rapid corkscrew motility
35
What is the pathogenesis of H.pylori?
◦Colonises gastric epithelial cells in stomach and metaplastic gastric epithelium in the duodenum or oesophagus.
◦Survives in mucus layer that coats epithelium and causes chronic inflammation of the mucosa.
◦The organism is non invasive but recruits and activates inflammatory cells.
◦H. pylori penetrate mucus layer lining of the stomach’s epithelium, attracted to chemotactic substances haemin and urea.
◦Recruits and activates inflammatory cells; they release urease that cleaves urea, producing NH3 that neutralises stomach acid and also to protect itself.
◦H. pylori cytotoxin and the ammonia produced by its urease cause destruction of the mucus-producing cells, exposing underlying connective tissues to stomach acid.
36
What tests are carried out to find H.pylori?
◦Blood antibody
◦Stomach biopsy
◦Stool antigen
◦Endoscopy
◦Urease breath test - Radioactively labelled urea is administered orally and if H. pylori is present in the patient’s stomach, the urease produced by the organism will split the urea to CO2, which will be radioactively labelled and then exhaled. The amount exhaled is measured.
37
What diseases are caused by H.pylori?
◦Acute gastritis
◦Stomach and duodenal ulcers
38
What is the treatment for H.pylori conditions?
A combination therapy of two or more antibiotics:
◦Amoxicillin
◦Clarithromycin
◦PPIs – Omeprazole
39
What is the structure of Hepatitis B?
Hepadnaviridae; It is divided into genotypes A-D.
* Circular DNA
* Partly double stranded and partly single stranded
* Non covalently closed genome with four overlapping genes
* Enveloped
* Icosahedral
* Multifunctional reverse transcriptase/DNA polymerase in virion
40
How is hepatitis B transmitted?
Infectious HBV is present in all body fluids of an infected individual – therefore blood, semen, saliva and breastmilk, for example, serve as sources of infection. In areas of high endemicity, the majority of the population becomes infected at or shortly after birth from a chronically infected mother or from an infected sibling. Individuals infected at a young age have a significant chance of becoming chronic carriers and they also have an increased risk of developing hepatocellular carcinoma later in life.
HBV is primarily a disease of infants in the developing world and in Western countries, it is mostly confined to adults who usually contract the infection through sexual intercourse or blood exposure from shared needles during IV drug use.
41
What is the pathogenesis of hepatitis B?
Fully differentiated hepatocytes are the primary cell type infected by HBV. The primary cause of hepatic cell destruction appears to be cell-mediated immune response, which results in inflammation and necrosis.
42
How does hepatitis B cause acute infections?
Following infection, HBV has a long but variable incubation period of between 45 and 120 days. Following this period, there is a prejaundice phase, characterised by mild fever, malaise, anorexia, myalgia and nausea. The acute icteric phase then follows and lasts for 1 to 2 months. During this phase, dark urine, due to bilirubinuria and jaundice are evident. The liver is usually enlarged and tender.
During the incubation period, HbsAg and HBeAg are the first indicators of a HBV infection and their presence indicates and active infection – however it does not distinguish between an acute and chronic infection.
Fulminant hepatitis: Where extensive necrosis of the liver occurs in 1-2% of the population with a HBV infection.
43
How does hepatitis B cause chronic infections?
The asymptomatic carriers of HBsAg are the most common type of persistently infected individuals. They usually have anti-HBeAg antibodies and little or no infectious virus in their blood.
Severe chronic hepatitis results in more frequent exacerbations of acute symptoms including progressive liver damage and potentially leading to cirrhosis and/or hepatocellular carcinoma.
Hepatocellular carcinoma typically appears many years after the primary HBV infection and the tumour itself is rather slow growing and only occasionally metastasises. Clinically, a patient exhibits weight loss, right upper-quadrant pain, fever and intestinal bleeding.
44
How is hepatitis B found in investigations?
* Elevation of ALTs, ASTs, bilirubin and prothrombin
* ELISA for detection of antigens and antibodies can distinguish between genotypes A-D
* Identification of specific antiviral antibodies and viral antigens permits differentiating between acute and chronic HBV infections
45
What is the treatment for hepatitis B infections?
In acute hepatitis, the immune system controls the infection and eliminates the virus in about 6 months. Drug therapy may be required with acute severe liver impairment that accompanies fulminant hepatitis.
The goal for treatment in patients with chronic hepatitis is to reduce the risk of progressive chronic liver disease and other long-term complications from chronic HBV such as cirrhosis and hepatocellular carcinoma. The most commonly used drugs include interferon-α or one of a large number of nucleoside/nucleotide antiviral agents e.g.:
* Adefovir
* Entecavir
* Tenofovir
46
What is the prevention for hepatitis B infections?
* Generalised and targeted vaccination
* Safe sexual intercourse
* Mother to child interventions (when the child is born, it will get vaccinated and immunoglobulins)
* Screening blood and products in healthcare
* Post exposure prophylaxis e.g. needlestick injury
47
What is the structure of Hepatitis C?
* Flaviviridae
* A positive strand, single-stranded, nonsegmented RNA genome.
* Enveloped
* Icosahedral
* Genomic RNAs serve as messenger RNAs and are infectious
* Virions do not contain any enzymes
48
How is hepatitis C transmitted?
* IV drug use
* Blood transfusion
* Patients on haemodialysis
* Tattoos
* Mother to infant
* Sexual intercourse
49
What is the pathogenesis of hepatitis C?
In the infected individual, viral replication occurs in the hepatocyte and in the lymphocytes and macrophages as well. Certain strains of HCV have been associated with hepatocellular carcinoma development, even in the absence of cirrhosis.
50
How do hepatitis C infection individuals present?
About 25% of infected individuals present with acute hepatitis and jaundice. Infections can progress to chronic hepatitis and cirrhosis and some of these individuals go on to develop hepatocellular carcinoma.
51
How is hepatitis C tested for?
* Reverse transcriptase of the viral RNA followed by PCR
| * Antibodies that react with a combination of recombinant viral proteins
52
What is the treatment for hepatitis C infections?
* IFN-γ plus ribavirin – cure rate is 40-80% as side effects are sometimes rate limiting
* No vaccine is available
53
How is hepatitis C prevented?
* Use of clean needles
* Generalised and targeted vaccination
* Safe sexual intercourse
* Mother to child interventions (when the child is born, it will get vaccinated and immunoglobulins)
* Screening blood and products in healthcare
* Post exposure prophylaxis e.g. needlestick injury
54
What is the structure of HIV?
* A lentivirus (which is a slow replicating retrovirus).
* A single stranded, positive-sense, linear RNA virus
* Has two copies per virion
* Enveloped
* Icosahedral
55
What are the two types of HIV?
There are two types of HIV, HIV-1 and HIV-2.
HIV-1 is more virulent, more infective and more widespread geographically, whereas HIV-2 is not as virulent and is localised exclusively to Western Africa.
56
How does HIV replicate?
1. Attachment to a specific cell surface receptor - bind to CD4 receptor. The virus infects helper T cells, lymphocytes, monocytes and dendritic cells.
2. Entry of the virus into the cell - chemokine receptor needed
3. Reverse transcription of viral RNA - after entering host cell, HIV RNA transcribed into DNA by reverse transcriptase. Reverse transcriptase cannot proofread, so errors often occur during conversion into DNA provirus.
4. Integration of the provirus into the host cell DNA - in nucleus, viral integrase cleaves chromosomal DNA and inserts provirus, becoming stable part of genome. The insertion is random. Therefore HIV has two genomic forms: single-stranded RNA present in the extracellular virus and proviral double-stranded DNA within the cell.
5. Transcription and translation of integrated viral DNA sequences - With host cell activation, DNA is transcribed to mRNA and viral genomic RNA. Viral mRNAs are translated to give viral enzymes and structural proteins.
6. Regulation - Rev and Tat proteins are made from spliced mRNAs, which prevent premature dissociation from the DNA template and transport out of the nucleus, bypassing the splicing machinery. This enables viral mRNAs to be correctly translated into polypeptides, which will be packaged into new virions.
7. Assembly and maturation of infectious progeny - As the virion buds from the surface, viral protease is activated and cleaves the polyproteins into their component proteins, which then assemble into the mature virion. Cleavage is a necessary step into the maturation of the infectious virus.
57
What is a chemokine receptor?
a cytokine with chemotactic properties, produced by lymphocytes and macrophages
58
How is HIV transmitted?
1. Sexual contact
2. Transfusions
3. Contaminated needles
4. Perinatal transmissions
59
How is HIV diagnosed?
* ELISA testing for the CA antigen in serum
* Calculating the viral load
* HIV-1 and 2 combined antibody and antigen test. There is a 25 day window between the time that the virus is present in the blood and when the antibody is present – therefore there can be false positives. Any positive result is confirmed using the Western blotting technique.
* Finding the resistance profile
* CD4+ levels
60
What is the treatment for HIV?
1.Early therapy
The steady state level of replicating virus in the plasma is a prognostic indicator of the rate of progression to AIDS. This has led to the principle that HIV infection should be treated aggressively and as early as possible, minimising the initial spread of the virus. There is also increased drug efficacy as drugs are administered at a time when mutants are still rare.
2.Highly active antiretroviral therapy (HAART)
This is multiple drug therapy. 3 different drugs are given at the same time, which act on different parts of the cell life cycle. This increases the chance of HIV resistance.
61
What is the absolute prevention for HIV?
* No sexual intercourse (even oral)
* Use of condoms
* Know your partner’s sexual history and infection status
* No IV drug use – but if so, use clean needles
* Healthcare products need to be screened
62
How do you reduce the risk of HIV infection?
•Mother to child transmission
◦Give mother HAART
◦Caesarian section reduces risk of transmission
◦No breast feeding (in developed world). If not, then breast feed for 6 months and then wean off the milk.
•Couples trying for a child
◦Give unaffected partner or both partners HAART to reduce risk of transmission to the child
63
What are clinical complications with HIV during latent periods?
i. Persistent, generalised lymphadenopathy
ii. Diarrhoea
iii. Chronic fevers
iv. Night sweats
v. Weight loss
vi. Rash
64
What are the stages of HIV infections?
1. Initial infection - The initially affected cells are the macrophages in the genital tract. From this, HIV disseminates via the blood and the virus may then localise in dendritic cells throughout the lymphoid tissue. From here, HIV can infect CD4+ lymphocytes.
2. Acute phase viraemia - Several weeks after the initial infection, some individuals experience an acute disease syndrome. During this period there is a high level of virus replication occurring in CD4+ cell. Antibody rests will not identify HIV-infected people.
3. Latent period - This lasts for months or many years following the acute infection. During this period, the majority of the HIV proviruses are transcriptionally silent. The infection remains relatively clinically asymptomatic as long as the immune system is functional.
65
What is the pathogenesis of HIV?
The pathology of HIV disease results from either tissue destruction by the virus itself or the host’s response to virus-infected cells. In addition, HIV can induce an immunodeficient state that leads to opportunistic diseases that are rare in the absence of HIV infection. Development from HIV infection to end-stage AIDS progresses through several phases.
66
What is the structure of the influenza virus?
* Negative stranded
* Single stranded
* Helical
* Enveloped
* Pleomorphic
* RNA is segmented into eight pieces
* Virion has two types of membrane protein spikes: H and N proteins
* Virion contains RNA polymerase
* Classified into A, B or C (A and B are medically important due to the H and N proteins and antigenic shift)
67
What is antigenic drift?
Random mutations in viral RNA and single or a small number of amino acid substitutions in H and N proteins
68
What is antigenic shift?
Occurs infrequently (e.g. every 10/20 years) and only happens with Influenza A. It is a change in the subtype of the H and/or N proteins. Reassortment of RNA segments result in a new virion different from parent virus.
69
How is the influenza virus transmitted?
* Respiratory droplets/Inhalation
| * Infection purely of the respiratory tract
70
What conditions does influenza virus cause?
•Influenza (‘the flu’)
◦Respiratory epithelial cells are destroyed by the host immune response via the cytotoxic T cells.
◦Acute onset characterised by chills followed by a high fever, muscle aches and extreme drowsiness
◦Runs for 4-5 days and then there is a gradual recovery
◦Pneumonia can occur in the very young, older adults and in those with chronic cardiac or pulmonary disease or who are immunodeficient
•Reye syndrome
◦Rare and serious complication of viral infections in children, especially in those who have had chickenpox or influenza.
◦Aspirin may contribute to the appearance of this syndrome therefore acetaminophen is prescribed for fevers of unknown origin.
71
What is the treatment for influenza infection?
* Amantadine and rimantadine prevent the influenza virus from uncoating and reduce symptoms but ONLY if given early in the infection.
* Zanamir
* Oseltamivir
72
How is influenza infection prevented?
* A vaccine consisting of formalin-inactivated influenza virus.
* A vaccine containing a live attenuated influenza virus can be administered intranasally.
73
What is found when testing for influenza virus?
* Quantitation of antibodies
* Viral antigens in respiratory tract
* PCR to detect viral RNA by reverse transcriptase
74
What is the structure of Neisseria meningitidis?
Stain: Gram negative
Shape: Diplococcus
Aerobic (obligate)
Encapsulated
75
What conditions does Neisseria meningitis cause?
◦Meningitis
| ◦Septicaemia
76
What happens in Meningitis?
The bacteria crosses the blood brain barrier where is multiplies and causes an acute inflammatory response. Joint symptoms and a petechial and/or purpuric rash are commonly observed. This can evolve into severe headaches, a rigid neck, vomiting and sensitivity to bright lights. Coma can occur within a few hours.
77
What is the pathogenesis of Neisseria meningitis?
Bacteria produce an IgA protease that cleaves IgA1 and thus evade the immunoglobulins of this class.
78
What are laboratory tests for Neisseria meningitis?
◦Sample of CSF
◦Culture on chocolate agar with CO2
◦Sugar utilisation tests – the pathogen uses both glucose and maltose
79
How is Neisseria meningitis transmitted?
Inhalation of respiratory droplets from a carrier or a patient in the early stages of the disease.
In addition to contact with a carrier, risk factors for the disease include recent viral or mycoplasma URTI, active or passive smoking and complement deficiency. In susceptible people, pathogenic strains may invade the bloodstream and cause systemic illness after an incubation period of 2 to 10 days.
80
What is the treatment for Neisseria meningitis infection?
◦Penicillin G
◦Cefotaxime
◦Ceftriaxone
Prophylactic Rifampicin is given to family members because of their inevitability of close contact. Other prophylactic treatment is oral ciprofloxacin and intramuscular ceftriaxone.
81
What is malaria?
Malaria is an acute infection disease of the blood, caused by one of the five species of the protozoal genus, Plasmodium, which is a sporozoan. P. falciparum account for some 15% of all malaria cases, and P.vivax for 80% of malarial cases.
82
What is the vector for the plasmodium genus?
Female Anopheles mosquito or infection, blood-contaminated needles, blood transfusion
83
How is plasmodium genus infection diagnosed?
Thick blood smears stained with Giemsa stain provide the most sensitive visual test. Thin blood smears, in which more details can be seen, are used to determine the species involved – which is important in planning a course of therapy. Serologic tests are usually too slow for diagnosis of acute diseases.
84
What is the treatment for infection by P.falciparum ?
* Quinine
* Artemisin
* Mefloquine
* Doxycycline
85
What is the treatment for infection by P.ovale or P.vivax?
* Initial treatment with chloroquine
* Then a two week course of primaquine (to achieve a ‘radical cure’ by eliminating the exoerythrocytic organisms that persist in the liver.
86
Why should patients be screened for G6PD deficiency before treatment with primaquine?
Individuals with this enzyme deficiency develop haemolytic anaemia, sometimes very severe, when treated with primaquine. This is due to the formation of methaemoglobin (Fe3+) rather than the ferrous haemoglobin (Fe2+).
87
What is the pathology for plasmodium genus?
Sporozoans reproduce asexually in human cells by a process called schizogony, in which multiple nuclear divisions are followed by envelopment of the nuclei by cell walls producing merozoites – these in turn become trophozites. Sexual reproductions occurs in the mosquito, where sporozoites are formed.
1. Infected mosquito injects sporozoites – infection can also result from use of a blood-contaminated needle or a blood transfusion.
2. Sporozoites migrate to the liver, where they form merozoites.
3. Merozoites are released and invade the blood cells, using haemoglobin as a nutrient.
4. In the red blood cell, the merozoite becomes a trophozoite.
5. In the red blood cells, the trophozoite multiplies, producing new merozoites. These are released when the red blood cell ruptures, and can infect other red blood cells.
6. Some merozoites become gametocytes – a cell that divides by meiosis to form gametes.
7. The female mosquito picks up gametocytes from an infected human. The sexual cycle occurs in the mosquito where sporozoites are formed.
If large numbers of red blood cells rupture at roughly the same time a sudden onset of fever can result from a massive release of toxic substances.
A predictable consequence of RBC lysis is anaemia, which is typical of Plasmodium infections.
88
Which is the most dangerous plasmodium species?
P.falciparum is the most dangerous plasmodium species as it can cause rapidly fulminating disease (as it invades both new and old red blood cells), characterised by persistent high fever and hypotension. Infection can lead to capillary obstruction and death if treatment is not prompt.
89
Which plasmodium species cause milder disease?
P.malariae, P.vivax, P.ovale cause milder forms of the disease, probably because they invade either new or old red blood cells, but not both.
90
What is the structure for proteus mirabilis?
Stain: Gram negative
Shape: Rods
Facultative anaerobe
Highly motile
91
What is the pathogenesis of proteus mirabilis?
◦Has the ability to produce high levels of urease. Urease hydrolyses urea to ammonia (NH3) and thus makes the urine more alkaline. If left untreated, the increased alkalinity can lead to the formation of crystals of calcium carbonate, and/or apatite.
◦The bacteria can be found throughout the stones, and these bacteria lurking in the kidney stones can reinitiate infection after antibiotic treatment. Once the stones develop, over time they may grow large enough to cause obstruction and renal failure.
92
What are laboratory findings for proteus mirabilis?
◦Dark in colour on blood agar and has a fishy smell
◦Alkaline urine sample
93
What diseases are caused by proteus mirabilis?
◦Wound infections
◦Septicemia
◦Pneumonias, mostly in hospitalized patients.
94
What is the treatment for proteus mirabilis?
◦Tetracycline
◦Cephalosporins
95
What is the structure of streptococcus viridans?
Stain: Gram positive
Shape: Cocci (chains)
Non-encapsulated
96
Where are Streptococcus viridans usually found?
They are commensal bacteria found in abundance in the mouth.
97
What diseases do streptococcus viridans usually cause?
◦If they are introduced into the bloodstream (e.g. dental extraction), they have the potential of causing endocarditis, particularly in individuals with damaged heart valves. They are the most common causes of subacute bacterial endocarditis.
◦They have the unique ability to synthesise dextrans from glucose, which allows them to adhere to fibrin-platelet aggregates at damaged heart valves.
◦Dental caries
98
What is the treatment for streptococcus viridans infections?
◦Vancomycin
◦Ceftriaxone
99
What is the structure of Pseudomonas aeruginosa?
Stain: Gram negative
Shape: Rod
Aerobic or facultative anaerobe
Encapsulated
100
What are the laboratory tests for Pseudomonas aeruginosa?
◦Produces blue and green pigments
◦Culture on MacConkey agar
◦Oxidase positive
◦Serology
◦Characteristic fruity odour
101
What is the pathogenesis for pseudomonas aeruginosa?
Pili on the bacteria mediate adherence. The alginate capsule is only expressed after a ‘patho-adaptive mutation’ occurs and this expression confers resistance to phagocytosis. It also produces numerous toxins and extracellular products that promote local invasion and dissemination of the organism.
102
What diseases are caused by pseudomonas aeruginosa?
Localised infections:
◦Swimmer’s ear
◦UTI
◦Abscess
Systemic infections:
◦Septicaemia
◦Bacteraemia
103
What is the treatment for pseudomonas aeruginosa infection?
```
Aggressive antibiotic therapy
◦β-lactams
◦Ceftazidime
◦Tobramycin
◦Ciprofloxacin
```
104
What is the structure of Salmonella enterica serovar typhi?
Stain: Gram negative
Shape: Rod
Facultative anaerobes
Ferment glucose and a wide range of carbohydrate
105
What is Salmonella enterica serovar typhi transmitted?
S. entrica serovar typhi is transmitted via the faecal-oral route, generally through food or water contaminated by human faeces. Young children and older adults are more susceptible to it, especially those living in crowded environments.
106
What is the pathogenesis of Salmonella enterica serovar typhi?
It causes disease by attaching to and invading the Peyer’s patches in GALT. The bacteria replicate rapidly within these cells and eventually spread to the liver and spleen causing hepatosplenomegaly.
107
What are the laboratory findings for Salmonella enterica serovar typhi?
◦Isolated from blood, faeces, bone marrow, urine
◦Cultured on MacConkey agar where it produces colourless, non-lactose fermenting colonies
108
What are the diseases caused by Salmonella enterica serovar typhi?
◦Typhoid fever
| ◦Enterocolitis - Contaminated poultry products including eggs
109
What is typhoid fever?
* A severe and life threatening illness, characterised by fever and abdominal symptoms.
* Rose spots on the trunk.
* After 1-3 weeks of incubation, can enter the blood resulting in bacteraemia causing fever, headache, malaise and bloody diarrhoea.
* Perforation of the intestine can cause haemorrhage.
110
What is the treatment for Salmonella enterica serovar typhi infection?
◦Ceftriaxone
◦Ciprofloxacin
◦Fluid and rehydration if diarrhoea is severe
111
What is the prevention against Salmonella enterica serovar typhi infection?
◦Attenuated live strain of S. enterica serovar Typhi
* One is oral
* The other is in a capsule and is delivered parenterally
112
What is the structure of Streptococcus pyogenes?
Stain: Gram positive
Shape: Coccus (chains)
Anaerobic
Encapsulated
113
What diseases are caused by streptococcus pyogenes?
◦Major cause of cellulitis
◦Acute pharyngitis
◦Impetigo
◦Purpural sepsis
114
What is the epidemiology for streptococcus pyogenes?
It can invade intact skin or mucous membranes causing some of the rapidly progressive infections known. A low inoculum suffices for infection. It does not survive well in the environment and is usually spread person to person by skin contact or via the respiratory tract.
115
What is the pathogenesis for streptococcus pyogenes?
The bacteria may simply replicate sufficiently to maintain themselves without causing injury – the patient is colonised at this point. Alternatively, the bacteria could grow and secrete toxins, causing damage to the surrounding cells, invading the mucosa and eliciting an inflammatory response.
116
What is the laboratory findings for streptococcus pyogenes?
◦Rapid latex antigen kits are used – in a positive test, the latex particles clump together.
◦Specimen samples can be obtained from throat swabs, pus and lesion samples, sputum, blood or spinal fluid.
◦They form small, opalescent colonies surrounded by β haemolysis on sheep blood agar.
117
What is the treatment for streptococcus pyogenes infection?
◦Penicillin G
◦Clarithyromycin
◦Azithromycin
118
What is the structure of Streptococcus pneumoniae?
Stain: Gram positive
Shape: Coccus (usually diplococcic but can be found as single/chained cocci)
Anaerobic
Encapsulated
119
What diseases are caused by streptococcus pneumoniae?
◦Community acquired pneumonia (CAP)
◦Adult bacterial meningitis – H.influenzae was the leading cause of bacterial meningitis but after a vaccine was created, S.pneumoniae became the most common cause.
◦Otitis media
◦Sinusitis
120
What is the epidemiology for streptococcus pneumoniae?
This bacterium is an obligate parasite of humans and can be found in the nasopharynx of many healthy individuals.
Infection can be endogenous where the carrier can develop an impaired resistance to the organism or other factors such as malnutrition, sickle cell disease leading to spleen removal or respiratory damage. They can also be exogenous where the infection can be spread via droplets from the nose of a carrier.
121
What is the pathogenesis for streptococcus pneumoniae infection?
The bacterial capsule is the most important virulence factor. It has antiphagocytic and antigenic properties. The cell associated enzymes pneumolysin and autolysin contribute to its pathogenicity.
122
What are the laboratory tests for streptococcus pneumoniae infection?
Specimens can be obtained from a nasopharyngeal swab, blood, pus, sputum or spinal fluid. α-haemolytic colonies appear (green colonies) when the bacterium is grown on blood agar overnight under aerobic conditions at body temperature. The cells are lysed by bile acids.
123
What is the treatment for streptococcus pneumoniae infection?
◦Penicillin G
◦Cephalosporins – Cefotaxime, Ceftriaxone
◦Vancomycin
124
How is streptococcus pneumoniae infection prevented?
◦Pneumococcal polysaccharide vaccine: protection of high risk individuals > 2 years
◦Pneumococcal conjugate vaccine: effective in infants and toddlers; 6 weeks to 5 years
125
What is the structure of Staphylococcus aureus?
Stain: Gram positive
Shape: Clustered cocci (in bunches like grapes)
Facultative Anaerobic
Encapsulated
126
What diseases are caused by staphylococcus aureus?
◦Skin and soft tissue infections
◦Osteomyelitis
◦Septic arthritis
◦Endocarditis
◦Septicaemia
◦Necrotising pneumonia
◦Toxic shock syndrome
◦Food poisoning
127
What is the treatment for staphylococcus aureus infection?
◦Oxacillin/Nafcillin
MRSA (healthcare associated)
◦Vancomycin
MRSA (acute and community acquired)
◦Trimethoprim/Doxycycline
MRSA (severe and community acquired)
◦Daptomycin/Vancomycin
128
What are the laboratory tests for staphylococcus aureus?
◦Testing for catalase
◦Strain strongly
◦Mannitol positive
◦Colonies tend to be yellow and haemolytic
◦Cultured on enriched media containing broth and/or blood
129
What is the pathogenesis for staphylococcus aureus?
Depends on the combined actions of the several virulence factors:
◦Cell wall virulence factors
◦Cytolytic exotoxins: referred to as haemolysins as they attack mammalian cell membranes
◦Superantigen exotoxins: they have an affinity for T cell receptor-MHC Class II antigen complex and stimulate an enhanced T-lymphocyte response. It can cause toxic shock by release of large amounts of T-cell cytokines.
◦Enterotoxins: these are a protein exotoxin that have an effect on the intestines by altering the apical membrane permeability of the intestinal epithelia. They are more heat stable than S. aureus therefore organisms are not always recovered from incriminated food but the toxin may be recovered.
130
Where is staphylococcus aureus usually found?
S. aureus is carried by healthy individuals on skin and mucous membranes. Carriers serve as a source of infection for themselves and others.
131
What are the characteristics of patients who get infected by staphylococcus aureus in hospitals?
Patients are typically elderly, debilitated, and/or chronically ill.
132
What is the infection site for staphylococcus aureus in hospital?
Bacteraemia commonly occurs with no obvious infection site. Infection of surgical wounds, open ulcer, intravenous line and urinary catheters often occur.
133
How is staphylococcus aureus transmitted in hospitals?
Occurs within healthcare settings. Rare in household contacts.
134
What is the medical history of patients who get infected with staphylococcus aureus in hospitals?
Infections are more likely in patients with a history of MRSA infections, recent surgery and admission to a hospital or nursing home. Antibiotic use, dialysis and permanent indwelling catheters are risk factors.
135
Why can vancomycin not be used again staphylococcus aureus
This is used to treat MRSA. However, in 1997, several MRSAs were isolated and found to have low-level vancomycin resistance, which has increased steadily resulting in the use of alternative drugs such as daptomycin.
136
Name Gram +ve cocci, diseases they cause, antibiotics for them and if vaccine is available (+/-)
Staphylococcus aureus
• Skin infections, pneumonia, meningitis, osteomyelitis, endocarditic, sepsis
• Penicillin
• -
Streptococcus pyogenes
• Pharyngitis, scarlet fever
• Penicillin
• -
Group B streptococci
• Pregnant women can pass onto child during birth, giving new born septicemia
• Penicillin
• -
Viridans streptococci
• Endocarditis if in bloodstream
• Cephalexin
• -
Streptococcus pneuominae
• Pneumonia, meningitis, sepsis, endocarditis, pericarditis
• Amoxicillin
• +
Enterorococci
• UTI, bacterial endocarditis, diverticulitis, meningitis
• Ampicillin
• -
137
Name Gram -ve cocci, diseases they cause, antibiotics for them and if vaccine is available (+/-)
Neisseria meningitidis
• Meningitis
• Ceftriaxone
• -
Neisseria gonnorrhoeae
• Gonnorrhoeae
• Ceftriaxone
• -
138
Name Gram +ve bacilli, diseases they cause, antibiotics for them and if vaccine is available (+/-)
Listeria
• Listeriosis
• Ampicillin
• -
Corynebacterium diphteriae
• Diptheria
• Penicillin
• +
Bacillus cereus
• food born illnesses, nausea, vomitting, diarrhoea
• Ciprofloxacin
• -
Clostridium perfringens
• Food poisoning
• Penicillin
• -
Clostridium difficle
• Diarrhoea
• Metronidazole
• -
Mycobacterium tuberculosis
• Tuberculosis
• Rifampicin
• +
Mycobacterium leprae
• leprosy
• Dapsone
• -
Non-tuberculous mycobateria
• Pulmonary disease
• +
139
Name Gram -ve bacilli, diseases they cause, antibiotics for them and if vaccine is available (+/-)
Escherichia coli
• Food poisoning, gastroenteritis
• Tetrocycline
• -
Salmonella spp
• Typhoid fever, gastroenteritis
• Ciprofloxacin
• -
Shigella
• Dysentery
• Ampicillin
• -
Klebsiella spp
• Pneumonia, UTI, Septicaemia
• cefotaxime
Proteus spp
• URI
• Ampicillin
• -
Pseudomonas aeruginosa
• Inflammation, sepsis
• Gentamicin
• -
Haemophilus
• Pneumonia, acute bacterial meningitis
• Cefrotaxime
• -
Bordetella pertussis
• Whopping cough
• Erythromycin
• +
Burkholdera spp
• pneumonia
• ceftazidime
• +
Brucella spp
• Brucellosis
• Doxycycline
• -
Legionella spp
• Legionnaire's disease
• lerofloxacin
• -
Vibrio cholerae
• cholera
• Tetracycline
• +
Campylobacter
• dysentery, peridontitis, diarrhoea
• azythromycin
• -
Helicobacter pylori
• peptic and duodenal ulcers
• amoxicillin
• +
Bacteroides spp
• peritonitis, appendicitis via abscess formation
• metronidazole
• -
Treponema pallidum
• syphillus
• penicillin
• -
140
Name other bacteria, diseases they cause, antibiotics for them and if vaccine is available (+/-)
Chlamydia spp
• Chlamydia
• Erythromycin
• -
Mycoplasma spp
• Pneumonia
•Tetracycline
• -
141
Name viruses, if they have RNA/DNA and enveloped or not, the diseases they cause, treatment for them and if there is a vaccine for them (+/-)
```
Poliovirus
• RNA non-enveloped
• Poliomyelitis
• no treatment
• -
```
```
Cocksackie (Enteroviruses)
• RNA non-enveloped
• Foot and mouth disease
• symptomatic
• -
```
```
Rhinovirus
• RNA non-enveloped
• common cold
• symptomatic
• -
```
```
Arbocirus encephalitis
• RNA enveloped
• Encephalitis
• Symptomatic
• -
```
```
Rubella
• RNA enveloped
• Rubella
• Symptomatic
• +
```
```
Measles
• RNA enveloped
• Measles
• Symptomatic
• +
```
```
Respiratory syncytial virus
• RNA enveloped
• Respiratory tract infection
• Symptomatic
• -
```
```
Rabies
• RNA enveloped
• Rabies
• Wash wound
• +
```
```
Influenza
• RNA enveloped
• Influenza
• Symptomatic
• +
```
```
Rotavirus
• RNA nonenveloped
• Gastroenteritis
• Symptomatic
• +
```
```
HIV
• RNA envelope
• AIDS
• Ciprofloxacin
• -
```
```
Adenovirus
• DNA non-enveloped
• URTI, gastroenteritis, conjunctivitis
• Symptomatic
• +
```
```
Papillomavirus
• DNA non-enveloped
• Papillomas
• Body's own immune system
• +
```
```
Herpes Simplex
• DNA enveloped
• skin blisters
• antiviral
• -
```
```
Epstein Barr virus
• DNA enveloped
• Hodgkins lymphoma
• symptomatic
• -
```
```
Cytomegalovirus
• DNA enveloped
• symptomatic on vulnerable people e.g. HIV
• Antiviral and symptomatic
• -
```
```
Hepatitis A
• RNA non-enveloped
• Hepatitis
• symptomatic
• +
```
```
Hepatitis B
• DNA enveloped
• Hepatitis
• Clears spontaneously
• +
```
```
Hepatitis C
• RNA enveloped
• Hepatitis
• Avoid alcohol and drugs
• -
```
```
Smallpox
• DNA enveloped
• smallpox
• symptomatic
• +
```
