Presented during HIV/AIDS Course Oct 2019 at Dept of Medicine, College of Health Sciences, Makerere University

1. HIV ASSOCIATED OPPORTUNISTIC
INFECTIONS OTHER THAN TB AND
CRYPTOCOCCOSIS
Presenters: Keneth Kananura & Pissi Singoma K (SHOs-1)
Facilitator: Dr. Ireen Andia B.
7th October 2019

2. Content Outline
• Introduction & classification
• Overview of different opportunistic infections (OIs)
• Treatment of OIs
• Prevention/prophylaxis
• END

3. Introduction
• Generally, there has been a dramatic decrease of HIV associated OIs due
to the introduction of ART.
• Most OIs are seen in patients with advanced HIV disease (CD4<200).
• Can be classified according to the causative agent: Bacterial, Viral,
Fungal, protozoal,
• Can be classified according to the system affected: Respiratory, GI,
CNS, or disseminated, etc.
At any
CD4 count
CD4 <300 CD4< 200 CD4< 100 CD4<50
TB Diarrhea from bacteria,
cryptosporidia,
microsporidia
Thrush
PCP
Bacterial
pneumonias
Toxoplasmosis
MAC infections
Crptococcosis
CMV infections.

4. Respiratory:
Pneumocystis Pneumonia(PCP)
• Caused by P jiroveci (formerly P carinii)
• Ubiquitous in the environment
• Initial infection usually occurs in early childhood
• PCP may result from reactivation or new exposure
• In immunosuppressed patients, possible airborne spread
• Generally there has been a decline in the incidence of PCP as a result of
ART and prophylaxis.
• Many patients who are diagnosed with PCP are unaware of their
underlying HIV infection.

5. RISK FACTORS
• CD4 count <200 cells/µL
• CD4 percentage <14%
• Prior PCP
• Oral thrush
www.hivbook.com/online
• Recurrent bacterial pneumonia
• Unintentional weight loss
• High HIV RNA
https://aidsinfo.nih.gov/guidelines

6. Pathophysiology of PCP
• Disease occurs when both cellular immunity and humoral
immunity are defective.
• Once inhaled, the trophic form of Pneumocystis organisms
attach to the alveoli.
• Multiple host immune defects allow for uncontrolled replication
of Pneumocystis organisms and development of illness.
• Activated alveolar macrophages without CD4+ cells are unable
to eradicate Pneumocystis organisms.
• Increased alveolar-capillary permeability is visible on electron
microscopy.

7. Pathophysiology …
• Physiologic changes include the following:
• Hypoxemia with an increased alveolar arterial oxygen
gradient
• Respiratory alkalosis
• Impaired diffusing capacity
• Changes in total lung capacity and vital capacity

8. Clinical Manifestations
 Symptoms
• Progressive exertional
dyspnea (95%)
• Fever (>80%)
• Nonproductive cough (95%)
• Chest discomfort
• Weight loss
• Chills
• Hemoptysis (rare)
 Signs
• Tachypnea
• Fever
• Tachycardia
• Crackles
• Nasal flaring
• Intercostal recessions
• cyanosis

9. Investigations
• Oxygen saturation (pulse oximetry)
• Arterial blood gas analysis
• CXR- perihilar infiltrates
• CT scan (HRCT)-indistinct diffuse changes including GGO
• 1,3-beta-D-glucan levels (elevated,>60pg/mL)
• LDH-high value is an unfavorable sign
• CD4 count/ HIV viral load
• Bronchoalveolar lavage-PCR, direct immunofluorescence assay,
microscopy
• CBC, AST/ALT, RFTs, should be done at baseline

10. Radiologic images in PCP
CXR-diffuse infiltrates HRCT shows GGO

11. Diagnosis
• Definitive diagnosis requires demonstrating organism:
• Induced sputum (sensitivity <50% to >90%)
• Spontaneously expectorated sputum: low sensitivity
• Bronchoscopy with bronchoalveolar lavage (sensitivity 90-99%)
• Transbronchial biopsy (sensitivity 95-100%)
• Open-lung biopsy (sensitivity 95-100%)
• PCR: high sensitivity for BAL sample; may not distinguish
disease from colonization

12. Microscopy
• Since Pneumocystis cannot be cultured, the gold standard for
diagnosis is microscopic visualization of the organism.
• Traditionally different stains have been used to identify either
the trophic form (Gram–Weigert, Wright–Giemsa or modified
Papanicolaou stains) or
• the cyst forms (calcofluor white,cresyl violet, Gomori
methenamine silver or toluidine blue)

13. Histopathology
Lung biopsy using silver stain to demonstrate P jiroveci
organisms in tissue
Credit: A. Ammann, MD; UCSF Center for HIV Information
Image Library

14. Treatment
GENERAL
• Treatment should be initiated immediately if there is clinical suspicion
• Oxygen support
• Start ART early (within 2 weeks)
SPECIFIC
• Preferred: TMP-SMX is treatment of choice
• Moderate-severe PCP
• TMP-SMX: 15-20 mg/kg/day TMP and 75-100 mg/kg/day SMX IV or PO in divided
doses Q6-8H
• Mild-moderate PCP
• As above, or TMP-SMX DS 2 tablets TID

15. Treatment…
• If IV CTX is not available, give Tab CTX 1920mg every 8 hours for 21 days.
• Corticosteroids
• Prednisone 40 mg BID days 1-5, 40 mg QD days 6-10, 20 mg QD days 11-21, or
methylprednisolone at 75% of respective prednisone dosage
• Alternative drugs: IV pentamidine, Clindamycin+primaquine
combination.
Prophylaxis (both primary &secondary): Daily co-trimoxazole
480mg is the drug of choice.
https://aidsinfo.nih.gov/guidelines

16. Bacterial pneumonias
• Risk factors: Detected viral load, CD4<500, Smoking, pre-existing lung
disease eg bronchiectasis, neutropenia, severe malnutrition, corticosteroid
therapy.
• Etiology: Community-acquired or nosocomial
Community-acquired: Streptococcus pneumonia, Hemophilus influenza,
Staphylococcus aureus, atypical pathogens like mycoplasma pneumonia,
Chlamydophila pneumonia, Legionella sp, etc.
Nosocomial pneumonia: S. aureus, Pseudomonas aeruginosa,
Klebsiella pneumonia, Enterobactor species, etc

17. Clinical manifestations
• Almost similar to that of HIV negative patients
• Most have an abrupt onset of fever, chills, cough, dyspnea, and chest pain
(may be pleuritic). Tachypnea, crackles, Dullness

18. Investigations
• CBC-Leucocytosis, neutrophilia
• Sputum analysis; Gram stain, ZN stain/Xpert
• Blood culture and sensitivity testing
• CXR-infiltrates, consolidations, effusions, etc
• HRCT scan: diffuse opacities, effusion, etc

19. Treatment
• Empirical treatment depending on clinical presentation.
• Initial antibiotic regimen will be directed at the most common
CAP pathogen.
• Treat as OPD or inpatient depending on the clinical status
• Abx examples include Amoxiclav, cephalosporins like
cefuroxime, ceftriaxone, cefixime, macrolides, etc.
• Prevention: Vaccinations, CTX prophylaxis, Smoking cessation
counseling.

20. MAC -associated infections
• These are caused by Mycobacterium avium complex-M. kansasii, M.
celatum,M. intracellulare, M. xenopi, etc
• Only patients with massive immunodeficiency & CD4 cells less than 50/µL
develop the disease.
• MAC pulmonary disease may include;
Cavitary disease in patients with underlying lung disease like COPD or
bronchiectasis
Nodular/bronchiectatic disease in patients without previously diagnosed
lung disease including non-smokers who invariably have bronchiectasis.

21. Clinical manifestation
• Cough (dry or productive)
• Fatigue/malaise
• Dyspnea
• Chest discomfort
• Hemoptysis
• Fever
• Weight loss
https://aidsinfo.nih.gov/guidelines

22. Disseminated MAC disease
• Anemia
• Elevated ALP
• Hepatomegaly, Splenomegaly, or
• Lymphadenopathy (paratracheal, retroperitoneal, paraaortic,or
less commonly peripheral)
• Localized syndromes include cervical, intraabdominal or
mediastinal lymphadenitis, pericarditis, osteomyelitis, skin or
soft tissue abscesses, bursitis, genital ulcers, or CNS infection.

23. Investigations & Treatment
Investigations:
• Blood cultures
• Alkaline phosphatase (↑)
• Sputum analysis
• CD4/ HIV RNA levels
• CXR
• CT scan
Treatment: Macrolide + Rifampin + ethambutol for 6-12 months

24. Toxoplasma pneumonia
• Caused by Toxoplasma gondii, an ubiquitous intracellular
protozoa.
• Most active cases of T. gondii in AIDS patients is due to
reactivation of latent infection.
• It occurs due to immunodeficiency, CD4 cells <100/µL.
• Clinical presentation: Fever, non-productive cough, dyspnea.
• Investigations: CXR (diffuse bilateral infiltrates), LDH,
Serology (IgG, IgM).
• Treatment:Pyrimethamine and Sulfadiazine combination, CTX,
Start ART.

25. Invasive Aspergillosis
• Is now uncommon but life threatening OI in AIDS patients.
• Caused by Aspergillus fumigatus.
• Invasive pulmonary aspergillosis is characterized by fungal
invasion into the lung parenchyma with pneumonia, with or
without dissemination to other organs like CNS, heart, kidneys
& sinuses.
• Risk factors: CD4<50 cells/µL, Neutropenia <500/mm3, steroid
use, underlying lung disease or opportunistic infection.
• Clinical manifestation: fever, cough, shortness of breath,
chest pain, hemoptysis.

26. Investigations and Treatment
Investigations:
• Culture (Sabouraud’s dextrose agar/Potato dextrose agar)
• Histopathology-septal hyphae with acute angle branching and
hyphae eroding into tissues
• Antigen detection
• 1,3, Beta-D-glucan
• DNA PCR
Treatment: Antifungal agents-Voriconazole, amphotericin B for
6-12wks, Start ART within two weeks.

27. PULMONARY HISTOPLASMOSIS
• Transmission occurs via inhalation of Histoplasma capsulatum
spores from soil contaminated with bird or bat excreta.
• Endemic areas include Mississipi, Caribbean, South America,
Africa, Asia.
• Risk factor: impaired cellular immunity, CD4,150 cells/µL
• Clinical presentation: Fevers, cough, night sweats, fatigue,
weight loss, dyspnea. PE: hepatosplenomegaly, LN
adenopathy, skin and mucosal lesions.

28. Investigations and Treatment
Investigations:
• CXR- focal infiltrates and mediastinal/hilar adenopathy
• CBC-pancytopenia
• Culture-blood, sputum or BMA
• Antigen testing (HPA)
• Direct microscopy-budding yeasts
• Serology
Treatment: Antifungal agents-amphotericin B + itraconazole

29. CNS INFECTIONS
 TOXOPLASMOSIS
• Its caused by the protozoan Toxoplasmosis gondii
• Most commonly found in those with CD4 cell counts lower than 100
cells/µL.
• Symptoms include headache, fever, and confusion. More advanced
encephalitis may cause seizures and coma. Visual disturbances.
• Signs may include focal weakness or stupor, cranial nerve palsy,
sensory deficits, aphasia, hemianopia, behavioral disorders.

30. Pathogenesis of Neurotoxoplasmosis
• Usually (95% of cases), results from reactivation of latent
bradyzoites cysts.
• With the immunosuppression, occurs the breakdown of tissue
cysts formed by the protozoa and the release of bradyzoites,
which multiply in place and later migrate to other organs.
• The injury is caused by cell invasion that starts a lytic process
and consequently leads to cell and tissue destruction.

31. Diagnosis
• A contrast-enhanced CT scan/MRI of the brain shows classic,
multiple ring-enhancing lesions.
• Serologic testing for antitoxoplasmosis immunoglobulin G
antibodies is helpful if the result is positive.
• The definitive diagnosis requires detection of the organism in
a clinical sample (e.g., brain biopsy)
• Most patients are given empiric therapy. Favorable response to
therapy, both clinically and radiologically, supports the
diagnosis.

32. MRI-T1 post contrast (Ring enhancement)

33. Treatment
• First-line therapy:
• Pyrimethamine 200 mg po loading dose followed by 75 mg/day
plus Sulfadiazine 1500mg PO QID.
• For sulfa allergic patients, pyrimethamine 200 mg po loading
dose followed by 75 mg/day plus clindamycin 600 to 1200mg IV
TID .
• Clindamycin plus SMX-TMP
• All pyrimethamine regimens should include folinic acid to
prevent drug-induced hematologic toxicity (10 to 25 mg/day po).

34. Alternative regimens:
• Used in patients unable to tolerate other medications:
• Pyrimethamine plus azithromycin (1200 to 1500 mg po qd)
• Pyrimethamine plus atovaquone (750 mg po qid)
• Sulfadiazine (1500 mg po qid) plus atovaquone (1500 mg po
bid)
Treatment is given for at least 6 weeks

35. Progressive Multifocal Leukoencephalopathy
• Caused by JC virus, a human polyomavirus
• It is a late manifestation of AIDS and is seen in ~1–4% of
patients with AIDS.
• The lesions of PML begin as small foci of demyelination in
subcortical white matter that eventually coalesce.
• The cerebral hemispheres, cerebellum, and brainstem may all
be involved.
Harrison’s Princ. Of internal Med, 20th Edition

36. Clinical presentation of PML
• Patients typically have a protracted course with multifocal
neurologic deficits, with or without changes in mental status.
• Motor deficits like hemiparesis or monoparesis, ataxia.
• Visual disturbances like diplopia, hemianopia.
• Seizures, aphasia, and sensory defects may occur.
• Headache, fever, nausea, and vomiting are rarely seen. Their
presence should suggest another diagnosis.

37. Pathophysiology
• When reactivation happens in the setting of immunosuppression,
viral replication ensues, causing dissemination to the brain.
• The viral infection of olingodendrocytes is lytic. Astrocytes are also
affected and may enlarge and take a bizarre shape.
• The virus infects other cells from a central nidus in a circumfrential
manner hence an expanding demyelinating lesion.
Medscape.com

38. Investigations
• MRI typically reveals multiple, nonenhancing white matter
lesions that may coalesce and have a predilection for the
occipital and parietal lobes.
• The measurement of JC virus DNA levels in CSF has a
diagnostic sensitivity of 76% and a specificity of close to 100%.

39. Treatment
• There is no specific treatment for PML; however, a median
survival of 2 years and survival of >15 years have been
reported in patients with PML treated with ART for their HIV
disease.
• Despite having a significant impact on survival, only ~50% of
patients with HIV infection and PML show neurologic
improvement with ART.

40. MRI (T2 weighted)

41. Ophthalmologic manifestations
 CMV Retinitis
• The majority of cases occur in patients with a CD4+ T cell count
<50/μL.
• Prior to ART era, this CMV reactivation syndrome was seen in 25–
30% of patients with AIDS but this has dropped to close to 2%.
• Usually presents as a painless, progressive loss of vision.
• Patients may also complain of blurred vision, “floaters,” and
scintillations.
• The disease is usually bilateral, although typically it affects one eye
more than the other.
Harrison’s Principles of internal medicine, 20th Edition

42. CMV Retinitis Cont…
• Diagnosis is made on clinical grounds by an experienced
ophthalmologist.
• Characteristic retinal appearance is that of perivascular
hemorrhage and exudate.
• CMV infection of the retina results in a necrotic inflammatory
process, and irreversible visual loss .
• May be complicated by retinal detachment as a consequence of
retinal atrophy in areas of prior inflammation.

43. Treatment and Prevention
• Therapy for CMV retinitis consists of oral valganciclovir, IV
ganciclovir, or IV foscarnet, with cidofovir as an alternative.
• If CMV disease is limited to the eye, intravitreal injections of
ganciclovir or foscarnet may be considered.
• Maintenance therapy to continue until CD4+ count remains
>100 μL for >6 months.
• Patients at high risk of CMV retinitis (CD4+ <100/μL) should
undergo an ophthalmologic examination every 3–6 months.

44. Oropharyngeal and GI infections
• Oral lesions, including thrush & hairy leukoplakia, are particularly
common in patients with untreated HIV infection.
• Thrush, due to Candida infection, and oral hairy leukoplakia, presumed
due to EBV, are usually indicative of fairly advanced immunologic decline,
CD4<300.

45. Oral Thrush
• Thrush appears as a white, cheesy exudate, often on an
erythematous mucosa in the posterior oropharynx.
• While most commonly seen on the soft palate, early lesions are
often found along the gingival border.
• The diagnosis is made by direct examination of a scraping for
pseudohyphal elements.
• Treatment: Antifungals like fluconazole, Nystatin suspension.
Harrison’s Principles of internal medicine, 20th Edition

46. Oral Hairly Leucoplakia
• Oral hairy leukoplakia presents as white, frondlike lesions,
generally along the lateral borders of the tongue and sometimes
on the adjacent buccal mucosa.
• Despite its name, oral hairy leukoplakia is not considered a
premalignant condition.
• Lesions are associated with florid replication of EBV.
• Treatment: topical podyphyllin,or antiherpesvirus agents

47. Esophageal Candidiasis
• Its common in HIV infected patients occurring at lower CD4
cells than Oropharyngeal candidiasis.
• Its caused mainly by Candida albicans.
• Generally presents with retrosternal burning pain or discomfort
along with odynophagia; occasionally can be asymptomatic.
• Endoscopic examination reveals whitish plaques similar to
those observed with oropharyngeal disease.
• On occasion, the plaques may progress to superficial
ulcerations of the esophageal mucosa with central or peripheral
whitish exudates.

48. Diagnosis & Treatment
• The definitive diagnosis requires direct endoscopic
visualization of lesions with histopathologic demonstration of
characteristic Candida yeast forms in tissue and confirmation by
fungal culture and speciation.
• Treatment: Systemic antifungals are required for effective
treatment.
• A 14- to 21-day course of either fluconazole (oral or intravenous
[IV]) or oral itraconazole solution is highly effective.
• No prophylaxis recommended.
https://aidsinfo.nih.gov/guidelines

49. Bacterial enteric infections
 Main pathogens
• Salmonella (particularly serotypes Typhimurium and Enteritidis),
• Shigella,
• Campylobacter
 Others include;
• Enteroaggregative E. coli
• Clostridium difficile
• Mycobacterium avium complex (MAC)

50. Enteric infection…
 Risk factors: Low CD4 <200 cells, Hospital exposure,
antibiotic use, HIV-associated alterations in mucosal immunity
or intestinal integrity and treatment with acid-suppressive
agents.
 Clinical Manifestation:
• Self-limited gastroenteritis;
• More severe and prolonged diarrheal disease, potentially
associated with fever, bloody diarrhea, and weight loss; and
• Bacteremia associated with extra-intestinal involvement, with or
without concurrent or preceding gastrointestinal (GI) illness.

51. Investigations & Treatment
• Investigations: Stool culture and sensitivity, C. difficile PCR,
endoscopy.
• RX: empiric antibiotics- Cipro, ceftriaxone, Hydration of the pt
(IV fluids).
• Prevention: Hand washing with soap, boiling drinking water,
avoiding contaminated food.,
https://aidsinfo.nih.gov/guidelines

52. Cryptosporidiosis
• Cryptosporidiosis remains a common cause of chronic diarrhea
in patients with AIDS in developing countries, with up to 74% of
diarrheal stools.
• Usually affects small intestines. With severe
immunosuppression, it can affect other parts of GI and extra GI
sites.
• Three commonly implicated species are Cryptosporidium
hominis, C. parvum, and C.meleagridis.
• Infection occurs through ingestion of Cryptosporidium oocysts.

53. Clinical manifestations
• acute or subacute onset of watery diarrhea, which may be
accompanied by nausea, vomiting, and lower abdominal
cramping.
• Fever is present in approximately one-third of patients,
• Malabsorption is common.
• The epithelium of the biliary tract and the pancreatic duct can
be infected with Cryptosporidium, leading to sclerosing
cholangitis and to pancreatitis secondary to papillary
stenosis.

54. Diagnosis & Treatment
• Diagnosis of cryptosporidiosis is by microscopic identification of
the oocysts in stool with acid-fast staining or direct
immunofluorescence, which offers higher sensitivity.
• RX: ART, Rehydration and electrolyte correction,
• Nitozaxanide (500-1000mg BID for 14 days)
• Prevention: hand washing, avoiding contaminated water and
food.
https://aidsinfo.nih.gov/guidelines

55. Cystoisosporiasis (Formerly Isosporiasis)
• Caused by Isospora (Cystoisospora) belli
• Infection results from ingestion of sporulated oocysts, such as from
contaminated food or water.
• After ingestion, the parasite invades enterocytes in the small
intestine. Ultimately, immature oocysts are produced and shed in
stool.
• The most common manifestation is watery (profuse), non-bloody
diarrhea, which may be associated with abdominal pain, cramping,
anorexia, nausea, vomiting, and low-grade fever.
• Acalculous cholecystitis and reactive arthritis also have been
reported.

56. Diagnosis
• Diagnosis: by repeated stool examinations with sensitive
methods, such as modified acid-fast techniques, on which
oocysts stain bright red, and UV fluorescence microscopy
• Rx: Clinical management includes fluid and electrolyte support
for dehydrated patients and nutritional supplementation for
malnourished patients.
• TMP-SMX is the antimicrobial agent of choice for treatment of
isosporiasis
• Prevention: avoiding potentially contaminated food or water
https://aidsinfo.nih.gov/guidelines

57. Hepatitis B Coinfection
• Its caused by HBV, partly double-stranded DNA.
• Its transmitted via sexual intercourse, blood, needles, mother-to-child
• A study done in Northern Uganda found a prevalence of HIV/HepB
coinfection at 6.7% (Ocama, Seremba, Apica & Opio, June 2015)
• According to UPHIA(2016), hepatitis B infection among adults is at
4.3% (5.6%men, 3.1% women, North(4.6%),South West (0.8%)
• Those with HIV/HBV coinfection have higher levels of HBV viremia
and lower likelihood of resolved infection following acute HBV
infection.
• Increased risk of HCC and liver-related mortality and morbidity.

58. Clinical Manifestations
• Acute HBV infection is asymptomatic in approximately 70% of
patients, and <1% of patients develop fulminant hepatic failure.
• When symptoms manifest, they may include RUQ abdominal
pain, nausea, vomiting, fever, and arthralgias with or without
jaundice.
• Most patients with chronic HBV infection are asymptomatic or
have nonspecific symptoms, such as fatigue.
• Between 15% to 40% of people with chronic HBV infection will
develop cirrhosis, hepatocellular carcinoma (HCC), or liver
failure. https://aidsinfo.nih.gov/guidelines

59. Diagnosis
• Serologic testing for surface antigen (HBsAg), hepatitis B core
antibody (anti-HBc total), and hepatitis B surface antibody (anti-
HBs)
• HBV e-antigen (HBeAg), antibody to HBeAg (anti-HBe), and
HBV DNA.
• Treatment: Patients with HIV/HBV coinfection should receive
tenofovir disoproxil fumareate (TDF)- or tenofovir alafenamide
(TAF)-based ART.
• Prevention: Vaccination, safe sex

60. Hepatitis C Virus Infection
• Caused by HCV, a single-stranded RNA Virus.
• Both HIV and HCV can be transmitted by exposure to blood or
blood products, through sexual intercourse, and from a mother
to her infant;
• HIV coinfection adversely affects the course of HCV infection,
resulting in significantly accelerated progression of liver disease
to cirrhosis, then end stage Liver disease particularly in those
with advanced immunodeficiency (CD4 count <200 cells/mm3).
• Prevalence of HCV in Uganda was found at 4.1% amongst
blood donors (Wolfang, Kataaha, et al 2006).

61. Clinical Manifestations
• Both acute and chronic HCV infections are usually minimally
symptomatic or asymptomatic.
• Fewer than 20% of patients with acute infection have low-grade
fever, mild RUQ pain, nausea, vomiting, anorexia, dark urine,
and jaundice.
• Unexplained elevations in serum ALT or AST levels may be the
only laboratory finding during acute and chronic infection.
https://aidsinfo.nih.gov/guidelines

62. Diagnosis & Treatment
• Tests: HCV antibody testing, HCV viral load testing
• Treatment: DAAS (Direct-acting antivirals) like daclatasvir,
elbasvir/grazoprevir, glecaprevir/pibrentasvir,
sofosbuvir/velpatasvir, etc.
• Be ware of drug-drug interactions between DAAS and ART.
http://www.hcvguidelines.org)

63. Dermatologic OIs
Bacillary angiomatosis (BA)
• BA is caused by either Bartonella quintana or Bartonella
henselae
• BA most often occurs late in HIV infection, in patients with
median CD4 T lymphocyte (CD4 cell) counts <50 cells/mm
• Development of BA lesions caused by B. henselae is
statistically linked to cat exposure in patients with HIV infection.
• In contrast, BA caused by B. quintana is associated with body
louse infestation and homelessness. The body louse serves as
the vector of B. quintana in humans

64. Clinical Manifestations
• BA lesions have been associated with nearly every organ
system,
• But cutaneous lesions are the most readily identified.
• Cutaneous lesions include papules, nodules, large friable
exophytic masses, large plaques.
• Visceral involvement-fever, chills, night sweats, weight loss,
symptoms of peliosis hepatis (abdominal pain, nausea,
vomiting)
https://aidsinfo.nih.gov/guidelines

65. BA (Pictures)

66. Diagnosis & Treatment
• Diagnosis can be confirmed by histopathology. BA lesions are
characterized by vascular proliferation, and a modified silver stain (such as
Warthin-Starry stain) usually demonstrates numerous bacilli.
• Treatment: Erythromycin 500 mg PO or IV q6h OR Doxycycline 100 mg
PO or IV q12h
• Therapy should be administered for ≥3 months
• Prevention: avoid rough play with cats and situations in which scratches
are likely, avoid contact with flea feces (i.e., flea dirt), and any cat-
associated wound should be washed promptly with soap and water.

67. Herpes Simplex Virus Disease
• Infections with human herpes simplex virus type 1 (HSV-1) and
type 2 (HSV-2) are common
• Approximately 70% of HIV-infected persons are HSV-2
seropositive and 95% are seropositive for either HSV-1 or HSV-
2
• HSV-2 infection increases the risk of HIV acquisition two- to
three-fold, and HSV-2 reactivation results in increases in HIV
RNA levels in blood and genital secretions of coinfected
patients.
https://aidsinfo.nih.gov/guidelines

68. Clinical Manifestations
• Orolabial herpes (e.g., cold sores, fever blisters) is the most
common manifestation of HSV-1 infection. Classic manifestations
include a sensory prodrome followed by the evolution of lesions from
papule to vesicle, ulcer, and crust stages on the lip.
• Genital herpes is the most common manifestation of HSV-2
infection. Typical genital mucosal or skin lesions evolve through
stages of papule, vesicle, ulcer, and crust.
• Local symptoms might include a sensory prodrome consisting of
pain and pruritis. Mucosal disease is occasionally accompanied by
dysuria or vaginal or urethral discharge.
• Inguinal lymphadenopathy is common with genital herpes,
particularly in primary infection

69. Diagnosis, Treatment
• HSV DNA polymerase chain reaction (PCR), and viral culture
are preferred methods. PCR is the most sensitive method.
• Prevention: Use of condoms consistently.
• Treatment: oral acyclovir, valacyclovir, or famciclovir for 5 to 10
days.

70. Varicella-Zoster Virus Disease
• Reactivation of latent VZV results in herpes zoster(shingles).
• Herpes zoster can occur in adults with HIV at any CD4 T lymphocyte
(CD4) cell count, but the risk of disease is higher with CD4
counts<200 cells/mm
• Clinical Manifestations:
• Varicella rash tends to have a central distribution with lesions first
appearing on the head, then the trunk, and finally the extremities,
evolving through stages of macules, papules, vesicles, pustules, and
crusts.
• New vesicle formation continues for 2 days to 4 days, accompanied
by pruritus, fever, headache, malaise, and anorexia

71. Herpes Zoster cont…
• Herpes zoster manifests as a painful cutaneous eruption in a dermatomal
distribution, often preceded by prodromal pain.
• The most common sites are the thoracic dermatomes (40% to 50%),
followed by cranial nerve (20% to 25%), cervical (15% to 20%), lumbar
(15%), and sacral (5%) dermatomes.
• Skin changes begin with an erythematous maculopapular rash, followed
by clear vesicles and accompanied by pain, which may be severe.
• New vesicle formation typically continues for 3 to 5 days. Crusts typically
persist for 2 to 3 weeks.
• Approximately 10% to 15% of patients with HIV report post-herpetic
neuralgia.

72. Diagnosis & Treatment
• PCR is the most sensitive and specific method.
• Treatment: the preferred treatment options are valacyclovir (1 g
PO three times daily), or famciclovir (500 mg PO three times
daily). Oral acyclovir (20 mg/kg max.of 800 mg five times daily)
• Prevention: avoid exposure to individuals with varicella or
herpes zoster & Vaccination.
https://aidsinfo.nih.gov/guidelines

73. END