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Year 2 CPEBLS > Mucosal infections > Flashcards

Mucosal infections Flashcards

1
Q

Describe syphilis in terms of:

  • Causative agent and description
  • Transmission
  • Disease description
A

Causative agent and description:
• Syphilis is an infection caused by the spirochaeteTreponema pallidum.
• Corkscrew-like
• Dies when exposed to air and temperature changes

Transmission:
• Sexual contact with someone who has active lesions
• Infected blood contact/ vertical transmission
• Requires a breach in mucosal membranes to invade host

Disease description:
• Has three stages; primary, secondary and tertiary infections

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2
Q

Describe syphilis in terms of:

- histological features of primary syphilis

A

Chancre:
• Ulcerated granulation tissue
• Dense mononuclear inflammatory cell infiltrate

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3
Q

Describe syphilis in terms of:

- histological features of secondary syphilis

A
  • Neutrophils in stratum corneum
  • Epidermal hyperplasia
  • Rete ridges thinning
  • Lymphocytic inflammation
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4
Q

Describe syphilis in terms of:

- histological features of tertiary syphilis

A

Gumma:
• Central area of coagulative necrosis well demarcated
• Peripheral zone of fibrosis = chronic inflammatory cells
• The causative microorganism, Treponema pallidum, cannot usually be found

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5
Q

Describe syphilis in terms of:

- clinical features of primary syphilis

A
  • Called chancre “shallow, painless ulcer with an indurated base”
  • Highly infections
  • Forms when the spirochete enters the body
  • Accompanied by regional lymphadenopathy
  • Heals spontaneously without treatment, then goes into latency
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6
Q

Describe syphilis in terms of:

- clinical features of secondary syphilis

A
  • Diffuse eruptions occur on the skin and mucous membranes
  • Very infectious

Oral lesions are known as mucous patches:
• Multiple
• Painless
• Greyish white plaques covering ulcerated mucosa

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7
Q

Describe syphilis in terms of:

- clinical features of tertiary syphilis

A
  • Appears as a firm mass that eventually becomes an ulcer
  • Called a gumma and is non-infectious, though it is a destructive lesion and can lead to perforation of the palatal bone (occur on tongue and palate)
  • Involve the cardiovascular system and the central nervous system
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8
Q

Describe syphilis in terms of:

- congenital syphilis

A

Description:
• Syphilis can be transmitted from an infected mother to the fetus (organism crosses the placenta)
• Causes serious and irreversible damage to the child, including facial and dental abnormalities

Oral consequences:
• Enamel hypoplasia
• Hutchinson’s incisors: affected incisors are shaped like screwdrivers: broad cervically and narrow incisally, with a notched incisal edge
• Mulberry molars: First molars appear as irregularly shaped crowns made up of multiple tiny globules of enamel instead of cusps

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9
Q

Describe tuberculosis in terms of:

  • Causative agent
  • Pathogenesis
A

Causative agent:
• Mycobacterium tuberculosis bacteria
• Travels in aerosol droplets. Bacteria have an affinity for the lungs

Pathogenesis:
• Bacteria lodge in the alveoli of the lungs
• After undergoing phagocytosis by macrophages, the organisms are resistant to destruction and multiply in the macrophages
• They then disseminate in the bloodstream.
• Primary tuberculosis: latent disease, asymptomatic
• Secondary tuberculosis: active disease, symptomatic

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10
Q

Describe tuberculosis in terms of:

- general clinical signs of tuberculosis (7)

A
  • Fever
  • Chills
  • Fatigue
  • Malaise
  • Weight loss
  • Persistent cough
  • May present with tuberculous lymphadenitis, most frequently affecting the cervical nodes
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11
Q

Describe tuberculosis in terms of:

- oral signs of tuberculosis (5)

A

Cause:
• They most likely appear when organisms are carried from the lungs in sputum and transmitted to the oral mucosa
• The tongue and palate are the most common sites for oral lesions

Lesion descriptions:
• Painful
• Not healing
• Slowly enlarging ulcers that are superficial or deep

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12
Q

Describe tuberculosis in terms of:

- histological features

A
  • Necrosis surrounded by macrophages
  • Multinucleated giant cells
  • Lymphocytes.
  • Langhan’s type giant cells
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13
Q

Describe tuberculosis in terms of:

  • mycobacterium bovis
  • atypical tuberculosis
A

Mycobacterium bovis:
• Source: infected milk
• Primary infection site: tonsils, mouth, intestine
• Only affects cattle
• Prevention: pasteurization of milk, cattle skin tested

Atypical tuberculosis
• Sources: soil, avium (poultry) or other mycobacterium species
• Most affected: Children, immune compromised

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14
Q

Describe candidiasis in terms of:

  • pathogenesis
  • histopathology
A

Pathogenesis:
• Candida albicansis the principal species associated with infection
• Commensal organism -> only causes disease in dysbiosis
• Occurs most commonly on tongue
• Commonly seen in new-borns, pregnant women, those who take antibiotics and those who are immunocompromised

Histopathology:
• Candidal hyphae invade the parakeratin more or less at right angles to the surface, but never penetrate deeper into the prickle cell layers

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15
Q

List the types of candida

A

Acute & Chronic pseudomembranous

Acute & Chronic Erythematous

Chronic Hyperplastic (pre malignant potential)

Candida Associated Denture Stomatitis

Candidal Angular Chelitis

Median Rhomboid Glossitis

Chronic Mucocutaneous

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16
Q

Describe deep visceral fungal infections in terms of:

  • pathogenesis
  • histopathology
  • oral signs (3)
A

Pathogenesis:
• All characterized by primary involvement of the lungs
• Oral lesions are caused by implantation of the organism carried by sputum from the lungs to the oral mucosa

Histopathology:
• Fungal hyphae

Oral:
• Chronic
• Nonhealing ulcers
• Resemble squamous cell carcinoma

17
Q

Describe deep visceral fungal infections in terms of:

- clinical signs (6)

A 
General:
• Fever
• Loss of appetite
• Lung: dry cough, can't breath, pain when breathing
• Bone: ulcer, infected skin
• Eye: visual blurring, red eyes
18
Q

Describe verruca vulgaris in terms of:

  • Pathogenesis
  • Clinical signs
A

Pathogenesis:
• “Common wart”
• Commonly occurs on skin
• The virus is inoculated by direct contact and may be transmitted from skin to oral mucosa.

Clinical:
• They appear white
• Seen in children
• May be sessile or pedunculated, single or multiple

19
Q

Describe verruca vulgaris in terms of:

- Histopathology

A
  • Projecting, papillary processes of epithelium
  • Acanthotic, hyperkeratotic squamous epithelium
  • Hyperplastic rete ridges around the margins usually slope inwards towards the centre of the lesion
  • Numerous cells with clear cytoplasm, called koilocytes, are present in the upper spinous layer of the epithelium
20
Q

Describe condyloma acuminatum in terms of:

  • Pathogenesis
  • Clinical signs
A

Pathogenesis:
• The virus is generally transmitted by sexual contact and is most commonly found in the anogenital region

Clinical:
• Papillary
• Bulbous masses
• Occurs: tongue, buccal mucosa, palate, gingiva, and alveolar ridge

21
Q

Describe condyloma acuminatum in terms of:

- Histopathology

A
  • Prominent acanthosis (thickened epithelium)
  • Finger like projections of epithelium
  • Marked broadening and elongation of the rete ridges
  • Keratinization is not a feature
22
Q

Describe herpes simplex infections in terms of:

- Pathogenesis (infection and latency)

A

Infection:
• Herpes virus infects an epithelial cell.
• There is degeneration and rupture of infected cells resulting in intraepithelial vesicles
• Rupture of cells releases new viral particles

Latency:
• During the primary infection, HSV gains access to sensory neurons and viral DNA is transported to the trigeminal ganglion.
• In the ganglion, transcription of HSV DNA is blocked, resulting in latency
Recurrence causes “secondary infection”

23
Q

Describe herpes simplex infections in terms of:

- Histopathology

A

Intact herpetic vesicle:
• Shows intra-epithelial blister/ pus
• The vesicle results from rupture of the virally infected epithelial cells caused by intracellular oedema
• Infected cells are swollen and have eosinophilic cytoplasm
• Giant cells form as a result of fusion of the cytoplasm of infected cells
• The lamina propria shows a variable inflammatory infiltrate

24
Q

Describe herpes simplex infections in terms of:

  • Clinical signs of primary herpes
  • Clinical signs of secondary herpes
A

Primary herpes
• Called primary herpetic gingivostomatitis
• Mainly in children
• Painful, erythematous, and swollen gingiva and multiple tiny vesicles on the perioral skin, vermilion border of the lips, and oral mucosa characterize the disease

Recurrent infection/ Secondary herpes:
• Called herpes labialis
• Stimuli: sunlight, menstruation, fatigue, fever, and emotional stress.
• Intra-orally, they resemble aphthous ulcers. Though, they appears on keratinized mucosa fixed to bone (hard palate and gingiva). The lesions appear as painful clusters of tiny vesicles or ulcers that can coalesce to form a single ulcer with an irregular border.

25
Q

Describe herpes zoster in terms of:

  • Pathogenesis
  • General clinical signs
  • Oral clinical signs
A

Pathogenesis:
• Cause by the varicella-zoster virus
• Primary infection: chickenpox
• Latent infection: herpes zoster/shingles
• In herpes zoster, any of the three branches of the trigeminal nerve may be affected: (1) the ophthalmic branch, (2) the maxillary branch, or (3) the mandibular branch

General clinical signs of herpes zoster:
• Skin lesions on the forehead/ eye occur when the ophthalmic branch is involved

Oral:
• Unilateral distribution
• Prodromal symptoms of pain, burning, or both, called paresthesia, often precede the development of vesicles
• Begin as vesicles that progress to ulcer
• Painful

26
Q

Describe hand, foot and mouth disease in terms of:

  • Pathogenesis
  • Histopathology
  • Clinical signs (general and oral signs)
A

Pathogenesis
• Coxsackievirus
• Predominantly in children and is transmitted in conditions of close association such as within households

Histopathology
• Neutrophil infiltrate

Clinical signs
General:
• Multiple macules or papules occur on the skin, typically on the feet, toes, hands, and fingers

Oral:
• Shallow, painful oral ulcers
• Occurs anywhere in mouth

27
Q

Describe herpangina in terms of:

  • Histopathology
  • Clinical signs
  • Oral signs
A

Histopathology:
• Oedema
• Intra-epithelial vesicle
• Epithelial necrosis and ulceration

Clinical signs:
• Fever
• Malaise 
• Dysphagia
• Sore throat

Oral:
• Vesicles, which rapidly break down into ulcers 1–2 mm in diameter, are seen on the tonsils, soft palate, and uvula

28
Q

Describe HIV infection in terms of:

  • Pathogenesis
  • Oral signs
A
  • Sore throat
  • Erythema of the buccal and palatal mucosa
  • Oral candidosis
  • Hairy leukoplakia
  • Kaposi’s sarcoma
  • Necrotizing periodontal disease
29
Q

Describe HIV infection in terms of:

  • AIDS
  • AIDS related complex
A

Acquired immune deficiency syndrome:
• Late stage of HIV infection, occurs when immune system is badly damages
• Number of their CD4 cells falls below 500 cells/mm3
• They develop one or more opportunistic infections regardless of CD4 counts

Aids related complex:
• Phase of infection with HIV that includes: low grade fever,unexplained weight loss, diarrhea, generalised lymphadenopathy
• Only used to describe people with HIV with mild symptoms

30
Q

Describe HIV infection in terms of:

  • Persistent generalised lymphadenopathy
  • HIV acute infection
  • HIV seropositivity
A

Persistent generalised lymphadenopathy:
• Known as enlargedlymphnodes (lymphadenopathy) in at least two areas of the body for at least 3 months
• Associated with early stages ofHIVinfection

HIV acute infection:
• Acute HIV infectionis the immediate period after HIV infection and refers to the first month after being infected
• In this early phase of infection, there is more risk of infecting others due to a high viral load

HIV seropositivity:
• Transmission of the virus may be followed by infection which is detected by the appearance of HIV antibodies
• This generally occurs within three months of exposure
• Most patients remain symptom-free for many years (HIV seropositive), but in time may develop persistent generalized lymphadenopathy
• Patients should get tested every 3 months. Their T-cell count should be above 500 and their viral load undetectable

Year 2 CPEBLS (6 decks)

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