Tirthankar Online: Mock test on Bacteriology (General and Systemic)

November 21, 2008

Mock test on Bacteriology (General and Systemic)

MICROBIOLOGY (BACTERIOLOGY) MOCK TEST

Full marks 40 Time – 2 hours

Attempt all questions. Supplement your answer with charts and diagrams as needed.

1. A middle aged lady attended the skin OPD with complaints of hypopigmented patch over the right elbow with progressive loss of sensation. What is your provisional diagnosis? How would you proceed to confirm the clinical diagnosis in the laboratory? How is the efficacy of treatment evaluated in such cases? [1 + 7 + 2]

Or, A middle aged person attended the STD clinic with a solitary painless ulcer with hard base on the glans penis. What is the commonest organism that causes such a lesion? What are the methods of isolation and demonstration of the organism in the laboratory? Discuss the role of serological tests in diagnosing late stages of the disease. [1 + 4 + 5]

Or, Name the bacteria responsible for diarrheal diseases in man. How would you proceed to investigate a case of bacterial diarrhea in the laboratory if you are supplied with the fresh fecal matter of the infected individual collected in a sterile plastic bottle? [2 + 8]

2. Write short notes on any THREE: [3 x 4 = 12]

a) Acid fast stain OR Bacterial growth curve
b) Plasmids OR Bacterial flagella
c) El Tor Vibrio OR Shiga toxin producing E. coli
d) Importance of ASO titer OR Interpretation of Mantoux test

3. Comment on any THREE: [3 x 4 = 12]

a) The choice of specimen for diagnosis depends on the stage of Enteric fever.
b) Koch’s postulates have many exceptions.
c) Morphology of the colonies of motile bacteria depends on the concentration of agar agar in Nutrient agar medium.
d) Bacteriological profile of purulent meningitis varies with the age of the patient.
e) Slide and tube coagulase tests are based on different biological principles.
f) Both chromosomal and extra-chromosomal factors are involved in the origin of bacterial drug resistance.

4. Differentiate between any THREE: [3 x 2 = 6]

a) Staphylococcus aureus and S. saprophyticus
b) Autoclaving and Tyndallisation
c) Streptococcus pneumoniae and Streptococcus pyogenes
d) Chlamydia and bacteria
e) Blood agar and chocolate agar

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Answers to your questions

2. Short note on SSSS.(Deborshi)

Ans:
Definition:

Staphylococcal scalded skin syndrome (SSSS) is an acute epidermolysis caused by a staphylococcal toxin.

Newborns and children are most susceptible. Symptoms are widespread bullae with epidermal sloughing. Diagnosis is by examination and sometimes biopsy. Treatment is antistaphylococcal antibiotics and local care. Prognosis is excellent with timely treatment.

Staphylococcal scalded skin syndrome (SSSS) almost always affects children < 6 yr (especially infants); it rarely occurs in older patients unless they have renal failure or are immunocompromised. Epidemics may occur in nurseries, presumably transmitted by the hands of personnel in contact with an infected infant or who are nasal carriers of Staphylococcus aureus. Sporadic cases also occur.
SSSS is caused by group II coagulase-positive staphylococci, usually phage type 71, which elaborate exfoliatin (also called epidermolysin), a toxin that splits the upper part of the epidermis just beneath the granular cell layer. The primary infection often begins during the first few days of life in the umbilical stump or diaper area; in older children, the face is the typical site. Toxin produced in these areas enters the circulation and affects the entire skin.

Symptoms and Signs

The initial lesion is usually superficial and crusted. Within 24 h, the surrounding skin becomes painful and scarlet, changes that quickly spread to other areas. The skin may be exquisitely tender and have a wrinkled tissue paper–like consistency. Large, flaccid blisters arise on the erythematous skin and quickly break to produce erosions. Intact blisters extend laterally with gentle pressure (Nikolsky's sign). The epidermis may peel easily, often in large sheets. Widespread desquamation occurs within 36 to 72 h, and patients become very ill with systemic manifestations (eg, malaise, chills, fever). Desquamated areas appear scalded. Loss of the protective skin barrier can lead to sepsis and to fluid and electrolyte imbalance.

Diagnosis

· Biopsy
· Cultures may be useful in adults

Diagnosis is suspected clinically, but confirmation usually requires biopsy (frozen section may give earlier results). Specimens show noninflammatory superficial splitting of the epidermis. In children, skin cultures are seldom positive; in adults, they are frequently positive. Cultures should be taken from the nose, conjunctiva, throat, and nasopharynx.

Differential diagnosis:

Differential diagnosis includes drug hypersensitivity, viral exanthemas, scarlet fever, thermal burns, genetic bullous diseases (eg, some types of epidermolysis bullosa), acquired bullous diseases (eg, pemphigus vulgaris, bullous pemphigoid), and toxic epidermal necrolysis. Stevens-Johnson syndrome is characterized by mucosal involvement, which is absent in SSSS.

Differentiating Staphylococcal Scalded Skin Syndrome (SSSS) and Toxic Epidermal Necrolysis (TEN)

SSSS

i)Patients affected - Infants, young children, immunocompromised adults

ii)Patient history - Recent staphylococcal infection, renal failure

iii) Level of epidermal cleavage (blister formation)* - Within the granular cell (outermost) layer of the epidermis

TEN

i)Patients affected - Older patients

ii)Patient history - Drug use

iii)Level of epidermal cleavage (blister formation)* - Between the epidermis and dermis or at the level of the basal cell

*Determined by Tzanck test or by a frozen section of a fresh specimen.

Treatment

· Antibiotics
· Corticosteroids not recommended
· Gel dressings for weeping lesions

With prompt diagnosis and therapy, death rarely occurs; the stratum corneum is quickly replaced, and healing usually occurs within 5 to 7 days after start of treatment.Penicillinase-resistant antistaphylococcal antibiotics given IV must be started immediately.

1. Comment: carcinoma usually spreads through lymphatics. (Himel)

Answer: It is a common dictum that carcinomas usually spread via lymphatics, and sarcomas usually spread through blood vessels. Most carcinomas metastasise by lymphatics, which include Ca breast, Ca stomach, Ca uterus, etc. However, it is not a universal dictum, as some Ca preferencially spreads via blood vessels, like renal cell carcinoma.

Recent research has thrown light on the probable reason behind this peculiar preference. The tumors that spread via blood vessels produce sufficient local angiogenesis, so that the tumor is well supplied by micro vessels that help in hematogenous spread. However, tumors that metastasise through lymphatics are rarely supplied with micro lymphatics. Instead, they have a surrounding chain of lymphatics outside the tumor mass. The spread into these vessels is facilitated if the surface area of the micro lymphatics can be increased or if the growth of intra-tumor lymphatics can be facilitated.. It is seen that the carcinomas that spread via lymphatics secrete higher amounts of VEGF-C, VEGF-D, VEGF-A and PDGF-BB, the growth factors that increase the number and the surface area of the lymphatics and facilitates the invasion by tumor cells. The higher expression of VEGF gene in carcinomas compared to sarcomas may explain why carcinomas more often spread via lymphatics.