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I am presenting here a brief description
of the HIV-hypothesis and a list of AIDS- defining diseases
as defined by the USA Centers for Disease Control and Prevention
(CDC) and the scientists at the National Institute of Health
(NIH)] to see if all of these illnesses really existed prior
to making HIV the cause of AIDS by the CDC in 1984 or whether
some of these diseases are rare or never occur in HIV negative
persons.
Pathology of AIDS as described by the CDC
The HIV-hypothesis states that HIV causes AIDS
by killing the CD4+ T cells directly or indirectly, and after
long incubation times (about 10 years), the number of these
cells will reach very low levels which lead to severe immune
deficiency. Patients with CD4+ T cells < 200/µL usually
suffer from opportunistic infections and certain forms of
cancer such as Kaposi’s sarcoma and lymphoma. The USA Centers
for Disease Control and Prevention (CDC) called the following
opportunistic diseases and cancers AIDS-defining diseases
when associated with low CD4+ T cells count (<500 /µL of
blood) [1,2]
The CDC’s list of AIDS-defining diseases:
A) Viral, bacterial, fungal, and yeast infections:
- Candididiasis, oropharyngeal (thrush), bronchi,
trachea, lungs, and vulvovaginal
- Listeriosis
- Toxoplasmosis of brain
- Histoplasmosis infection
- Isosporiasis
- Mycobacterium tuberculosis
- Pneumocystis carinii pneumonia
- Herpes zoster
- Cytomegalovirus.
- Bacillary angiomatosis
- Cryptococcosis
- Cryptosporidiosis
- Isosporiasis
- Salmonella septicemia, recurrent
- Pneumonia, recurrent
B) Idiopathic and inflammatory conditions:
- Diarrhea lasting more than one month
- Wasting disease
- Idiopathic thrombocytopenic purpura
- Peripheral neuropathy
- Encephalopathy
- Progressive multifocal leukoencephalopathy
- Pelvic inflammatory disease, particularly
if complicated by tuboovarian abscess.
- Hairy leukoplakia, oral
C) Cancer
- Cervical dysplasia and carcinoma in situ
- Cervical cancer invasive
- Kaposi’s sarcoma
- Lymphoma, Burkitt’s (or equivalent term)
- Lymphoma, primary, of brain
My evaluation of the medical literature revealed
that the list of opportunistic infections presented above
are also described in patients receiving organ transplants
and patients with chronic illnesses who are treated chronically
with high doses of corticosteroids and other immunosuppressive
agents and in people suffering from malnutrition. These illnesses
have been reported prior and after the appearance of AIDS
epidemic in the USA in 1981 in HIV-negative and HIV-positive
individuals. In addition, some of the illnesses on the CDC’s
list such as pelvic inflammatory disease, cervical dysplsia,
and cervical cancer have been reported in women with normal
immune system [1,2]. Below are the descriptions of seven of
these illnesses that are called AIDS-defining diseases by
the CDC and the pathology of malnutrition in relation to the
immune system to illustrate my points. The epidemiology and
the pathology of other diseases on the CDC list are described
in Al-Bayati’s book [1] and Fauci et al.’s book [2].
Tuberculosis (TB)
Tuberculosis (TB) is caused by Mycobacterium
tuberculosis and is one of the diseases listed by the
CDC as an AIDS-defining disease[1,2]. This disease has been
known for more than one thousand years. It occurs most commonly
in people suffering from malnutrition, cancer, diseases of
the immune system, people treated chronically with immunosuppressive
agents, and in illicit drug users. There is overwhelming published
information demonstrating that HIV has nothing to do with
TB. The best medical evidence to prove these points is presented
by Fauci et al. [2].
Briefly, Fauci et al. reported that "TB is one
of the oldest diseases known to effect humanity. This has
been proved by the findings of tuberculous spinal disease
in Egyptian mummies. During the industrial revolution and
the period of related urbanization in the seventeenth and
eighteenth centuries, tuberculosis became a problem of epidemic
proportions in Europe, causing at least 20 percent of all
deaths in England and Wales in 1650. In the eastern part of
the United States, the annual mortality rate from tuberculosis
in the early nineteenth century was approximately 400 per
100,000 population". They also stated that "approximately
3.8 million new cases of tuberculosis, 90 percent of them
from developing countries, were reported to the World Health
Organization in the early 1990s. However, because of a low
level of case detection and poor reporting in many national
programs, reported cases represent only a fraction of the
total. It is estimated that 8.8 million cases of tuberculosis
occurred worldwide in 1995, 95 percent of them in developing
countries of Asia (5.5 million), Africa (1.5 million), the
Middle East (747,000). It is also estimated that nearly 3
million deaths from tuberculosis occurred in 1995 and 98 percent
of them in developing countries"[2]. Sheik et al. examined
183 cases of lymphadenopathy involving various sites in Indian
children and they found that 49.2% proven to be of tubercular
origin [3].
Fauci et al. also stated that "the risk of developing
TB after being infected depends largely on endogenous factors,
such as the individual’s innate susceptibility to diseases
and level of function of cell-mediated immunity. Clinical
illness directly following infection is classified as primary
tuberculosis and is common among children up to 4 years of
age. This form is often severe and disseminated. Dormant bacilli,
however, may persist for years before being reactivated to
produce secondary tuberculosis, which is often infectious.
Overall, it is estimated that about 10% of infected persons
will eventually develop active tuberculosis. Conditions known
to increase the risk of active tuberculosis among persons
infected with tubercle bacilli include silicosis; lymphoma,
leukemia and other malignant neoplasm; hemophilia; chronic
renal failure and hemodialysis; insulin- dependent diabetes
mellitus; immunosuppressive treatment; and conditions associated
with malnutrition"[2].
Furthermore, the risk factors in drug users
of getting pneumonia and TB were also explained by Fauci et
al. as follows: "Community-acquired bacterial pneumonia was
commonly described among drug users. The putative risk factors
in drug users included pulmonary aspiration resulting from
intermittent overdose, deleterious effects of opiates on lung
defenses and cough reflex, hypoventilation due to respiratory
depression and smoking. The other important pulmonary infection
described in drug injectors is tuberculosis. Infections due
to M. tuberculosis were well documented in drug users
before the AIDS epidemic, accounting for greater morbidity
and mortality in this population than in the non-drug-using
population. Although some authors attributed this greater
impact to poverty, poor housing, and the social and demographic
factors associated with both drug use and tuberculosis, others
found an elevated risk of tuberculosis among drug users even
after attempting to control for these other factors. There
is also evidence that tuberculous meningitis and focal tuberculomas
of the brain may be more common among drug users than other
patients with tuberculosis, with or without HIV infections.
Finally, ocular infections have been well described in drug
injectors" [2].
In addition, the standard treatment for TB in
patients with AIDS are glucocorticoids and isoniazid. The
side effects of isoniazid are hepatitis, peripheral neuritis
and optic neuritis. Peripheral neuropathy is considered one
of the AIDS-defining disease by the CDC and the treatment
for peripheral neuropathy is glucocorticoids [1,2,4,5,6].
The doses of glucocorticoid that are given to a patients with
AIDS can cause AIDS in a healthy person [1,2,4,5,6].
Pneumocystis carnii pneumonia (PCP)
PCP is one of the opportunistic infection classified
by the CDC as an AIDS-defining disease. My review of the medical
literature shows that this disease exist prior to HIV and
has nothing to do with it . It occurs as a result of the use
of local and/or systemic immunosuppressive agents, malnutrition,
and other diseases that effects the immune system [1]. The
predisposing factors for PCP were described by Fauci et al.
[2]. Briefly, they stated that Pneumo-cystis carinii
is an opportunistic pathogen whose natural habitat is the
lung. The organism is an important cause of pneumonia in the
compromised host. P. carinii pneumonia occurs in premature
and malnourished infants; children with primary immunodeficiency
diseases; and patients receiving immunosuppressive therapy
(particularly glucocorticoids) for cancer, organ transplantation,
and other disorders. Symptoms often began after the glucocorticoid
dose has been tapered.
Jones et al. reviewed the medical records of
15,558 homosexual men and 4475 drug users. They found that
6.8% and 8.3% of homosexuals and drug users had PCP, respectively[7].
Sepkowitz et al. conduced a twelve-year retrospective review
from a tertiary-care cancer center that included 134 HIV-negative
cancer patients. Corticosteroids were found to be a significant
risk factor for PCP in 116 (87%) of these patients. The median
maximum corticosteroid dose was 80 mg prednisone and the median
length of time receiving corticosteroids was 3 months [8].
In addition, Caiaffa et al. examined the risk factors for
the first episode of bacterial pneumonia among 40 HIV-seropositive
injection drug users (IDUs) and found that the most distinctive
behavioral characteristic among these patients associated
with an increased odds of bacterial pneumonia was the practice
of smoking drugs other than cigarettes (marijuana, cocaine,
crack). The association of smoking illicit drugs with bacterial
pneumonia was independent of the level of immunosuppression,
age, and cigarette smoking. Habitual marijuana smoking is
also associated with chronic respiratory symptoms but causes
functional impairment with chronic respiratory symptoms predominantly
in large airways[9].
Recurrent pneumonia
Recurrent pneumonia caused by Streptococcus
pneumoniae and Haemophilus influenzae is considered
an AIDS-defining disease by the CDC. It has been very well
documented that this disease can occur in any individual (HIV-positive
or HIV-negative) if the conditions are favorable such as smoking,
crowded environments such as gay bars, use of drugs, malnutrition,
use of steroids. etc. These facts have been known for more
than 100 years prior to the appearance of AIDS in America
[1,2].
Fauci et al. [2] stated that "Streptococcus
pneumoniae was recognized as a major cause of pneumonia
in the 1880s and has been central focus of study to modern
understanding of humoral immunity. S. pneumoniae colonizes
the nasopharynx and can be isolated from 5 to 10 percent of
healthy adults and from 20 to 40 percent from healthy children.
Pneumococci spread from one individual to another as a result
of extensive close contact; transmission may be enhanced by
poor ventilation. Day-care centers have been a site of spread
of penicillin-resistant stains. Epidemics among adults are
associated by with crowded living conditions-e.g., in military
barracks, prisons, and shelters for the homeless. The incidence
of pneumoccocal bacteremia is relatively high among infants
up to 2 years of age and low among teenagers and young adults;
rates increase steadily beginning at around age 55. The incidence
of pneumococcal bacteremia among adults exhibits a distinct
midwinter peak and a striking dip in summer. The predisposing
factors for Streptococcus infection are glucocorticoid
treatment, defective antibody formation, malnutrition, alcoholism,
infancy and aging, cigarette smoking. Etc"[2].
Candidiasis
Candidiasis of the vagina can occur even in
normal women, women treated with antibiotics, and in diabetic
patients [1,2]. Fauci et al. stated that candidiasis is often
preceded by increased colonization of the mouth, vagina, and
stool with Candida due to broad-spectrum antibiotic
therapy and additional local and systemic factors favor infection.
Oropharyngeal thrush particularly occurs in neonates and in
patients with diabetes mellitus. Vulvo-vaginal candidiasis
is especially common in the third trimester of pregnancy.
Candida from the perineum can enter the urinary tract
via an indwelling bladder catheter. Cutaneous candidiasis
most often involves macerated skin, such as that in the diapered
area of infants, under pendulous breasts, or on hands constantly
in water or covered by occlusive gloves. Intravenous drug
abuse or third-degree burns can also provide a skin portal
for Candida that can lead to deep candidiasis. Once
Candida has passed the integmentary barrier, hematogenous
seeding is particularly evident in the retina, kidney, spleen,
and liver in very low birth weight babies ( neonates) and
in patients suffering from neutropenia or use glucocorticoid
therapy that markedly decrease host defense[2]. Belcomethasone
dipropionate (glucocorticoid aerosol) is used to treat asthma
and chronic respiratory infection in drug users, homosexuals,
and heterosexuals. Localized infections with Candida albicans
or Aspergillus niger have occurred in the mouth and
pharynx and occasionally in the larynx. Positive culture for
oral Candida may be present in up to 75% of patients.
Glucocorticoid aerosols also have systemic side effects[1,4].
Histoplasmosis
This disease caused by a fungus found in the
soil and effects healthy children and adults and immunocomprised
hosts. It has been reported prior to the discovery of HIV.
Its inclusion as an AIDS-defining disease by the CDC is a
big puzzle to me and probably to any person who reads the
description provided by Fauci et al. stated below [2].
Fauci et al. reported that "Histoplasmosis is
a disease cause by Histoplasma capsulatum (fungus).
Infection has been encountered in many areas of the world
but is much more frequent in certain areas. Endemicity is
probably contingent on the availability of proper conditions
in nature for growth of the fungus. H. capsulatum prefers
moist surface soil, particularly soil enriched by droppings
of certain birds and bats. It is an opportunistic disease
endemic to the Mississippi and Ohio River valleys, Puerto
Rico, the Dominican Republic, and South America. Many case
clusters have occurred 5 to 18 days after the exposure of
groups of people to dust, while cleaning dirt-floored chicken
coops, bulldozing, or cave exploring. Skin-test-reactivity
in many endemic areas indicates that 80 percent or more of
residents over age 16 have been exposed. Microconidia, or
small spores, of H. capsulatum are small enough to
reach the alveoli upon inhalation and begin to bud there.
With time, an intense granulomatous reaction occurs. Caseation
necrosis or calcification may mimic tuberculosis. Chronic
pulmonary infection favors otherwise healthy males over the
age of 40. A history of cigarette use is elicited from nearly
all patients with chronic progressive pulmonary histoplasmosis.
An acute, rapidly fatal course is most likely to be encountered
among young children and immunosuppressed patients, including
those with AIDS. The symptoms of acute infection include fever,
emaciation, hepatosplenomegaly, lymphadenopathy, jaundice,
anemia, leukopenia and thrombocytopenia. Chronic but equally
lethal disseminated infection is more common among previously
healthy adults"[2].
In addition, thrombocytopenia is one of the
symptoms of acute histoplasmosis. Recall that this is also
an AIDS-defining disease and the standard treatment for thrombocytopenia
is glucocorticoids and immunosuppressive agents as described
by Fauci et al. [2].
Cervical Cancer and Pelvic Inflammatory Disease
(PID)
Diseases of the reproductive system are very
common and were known prior to the AIDS era. They have no
relation or any connection to HIV. They have been caused by
sexually transmitted and nonsexually transmitted infectious
agents and may be other factors and their occurrence is dependent
on many physiological and environmental factors. They occur
in women with or without immune deficiency. Adding these diseases
to the list of AIDS-defining diseases is not supported by
any scientific facts and it also made the picture of AIDS
more complicated and horrifying.
A) Pelvic Inflammatory Disease (PID):
The CDC considered PID, particularly if complicated
by tuboovarian abscess as an AIDS-defining disease with no
medical justification. This disease is caused by very common
infectious agents and drug use. Gonococcal infection and other
sexually and nonsexual transmitted bacterial, viral, fungal
infections, parasitic infections cause PID in immunocompromised
women and in women with normal immune systems. The CDC in
Atlanta estimates that at least 12 million U.S. residents
acquire a sexually transmitted disease (STD) per year. Some
authorities estimated that at least half of all Americans
acquire a sexually transmitted infection by age 35. Fauci
et al. stated that "about 850,000 cases of PID occurred per
year during the mid 1970s and this period is prior to the
AIDS epidemic [2].
Rubin and Farber reported that inflammation
of the cervix is exceedingly common and is related to its
constant exposure to the bacterial flora in the vagina. Acute
and chronic cervicitis result from infection with many microorganisms,
particularly the endogenous vaginal aerobes and anaerobes,
Streptococcus, Staphylococcus, and Enterococcus,
Neisseria gonorrhoeae, and Herpes simplex type 2. Some
agents are sexually transmitted, whereas others may be introduced
by foreign bodies, such as residual fragments of tampons.
Excluding N. gonorrhoeae, Streptococcus and
Staphylococcus are usually encountered after parturition[10].
In addition, Fauci et al. presented a list of
pathogenic agents on page 813 of their book [2] that cause
pelvic inflammatory diseases in women and HIV is not among
them. They stated that acute PID is almost exclusively a diseases
of active women. Important risk factors include a history
of salpingitis, a recent history of vaginal douching, and
the use of an IUD, particularly the Dalkon shield. Factors
cited as possibly contributing to intracanalicular upward
spread of gonococci and chlamydiae from the endocervix to
endosalpnix include estrogen dominated cervical mucus, attachment
to sperm that migrate upward into the tube, use of an IUD,
vaginal douching, and menstruation. The onset of symptoms
of N. gonorrhoeae-associated and C. trachomatis-associated
PID often occurs during or soon after the menstrual period.
Furthermore, the effects of alcohol and illicit
drugs on the function of the reproductive system in females
are very extensive. Fauci et al. reported that the repeated
ingestion of high doses of ethanol by women can result in
amenorrhea, decrease in ovarian size, absence of corpora lutea
with associated infertility and spontaneous abortions. Women
who abuse cocaine have reported major derangement in menstrual
cycle function, including galactorrhea, amenorrhea, and infertility.
Chronic cocaine abuse may cause persistent hyperprolactinemia
as a consequence of cocaine-induced disorders of dopaminergic
regulation of prolactin secretion by the pituitary. Cocaine
abuse, particularly the smoking of crack by pregnant women,
has been implicated in causing an increased risk of congenital
malformations and of perinatal cardiovascular diseases in
the mother [2]. The only relation between HIV and PID is that
they both may be acquired by sexual transmission. Otherwise,
PID is an individual entity, not a result of HIV [1].
B) Cervical Dysplasia and Cancer
The CDC also included cervical dysplasia and
cervical cancer as AIDS indicator diseases in women. These
diseases have nothing to do with HIV. These illnesses have
been reported in women with normal immune function and women
having immune depression [2,10]. Fauci et al. stated that
"Carcinoma of the cervix was once the most common cause of
cancer death in women, but over the past 30 years, the mortality
rate has decreased by 50 percent. In 1996, there were approximately
15,700 new cases of invasive cervix cancer, and more than
50,000 cases of carcinoma in situ. The disease remains the
major gynecologic cancer in underdeveloped countries. It is
more common in lower socioeconomic groups, women with early
initial sexual activity, multiple sexual partners, and in
smokers. Many of these factors suggest a venereal transmission.
It appears that the human papillomia viruses (HPV) has an
important etiologic role. Uncomplicated HPV lower genital
tract infection and condylomatous atypia of the cervix can
progress to cervical intraepithelial neoplasia (CIN). This
lesion precedes invasive cervical carcinoma and is classified
as low-grade squamous intraepithelial lesion (SIL), high grade
SIL, and carcinoma in situ. Carcinoma in situ demonstrates
cytologic evidence of neoplasma without invasion through the
basement membrane, can persist unchanged for 10 to 30 years,
but eventually progresses to invasive carcinoma" [2].
It has been also reported in a standard pathology
text book that, fifty years ago, cervical cancer was the leading
cause of cancer death in American women [10]. With the introduction
and widespread application of cytologic screening, the incidence
of invasive cervical cancer has been halved and the mortality
rate has dramatically decreased. The Papanicolaou smear detects
premalignant diseases long before invasion has occurred. Even
one smear during a women’s lifetime (which is clearly inadequate),
reduces the risk of invasive cancer 10-fold. Cervical cancer
remains an important cause of cancer mortality in the United
States. With improved surveillance, there has been a marked
increase in the incidence of its precursor lesions, cervical
intraepithelial neoplasia (CIN), also known as cervical dysplasia
and carcinoma in situ. Squamous cell carcinoma is by far the
most common type of cervical cancer. Despite its declining
frequency in the United States, it still has an incidence
of 13,000 new cases annually (15 new cases annually per 100,000
women). By contrast, In Central and South America, parts of
Asia, and Africa, squamous cell cancer of the cervix remains
a major cause of cancer death. In some high-risk areas, its
incidence is 100 new cases annually per 100,000 women [10].
Malnutrition and AIDS
It has been stated that the finding of atrophy
of lymphoid tissue in people suffering from malnutrition was
observed as early as 1925. For example, Jackson’s review on
this topic in 1925 noted that many investigators had found
a pronounced tendency of atrophy of lymphoid tissue in all
conditions of malnutrition. Thymus weight was exquisitely
sensitive to malnutrition and was earlier designated as the
"barometer of nutrition [11].
I have found an extensive literature describing
the impact of malnutrition on the function and the structure
of the immune system in people in Africa. This information
clearly demonstrates that AIDS in Africa is caused by starvation
and not by HIV. The functions of the immune system, especially
the cellular immunity, are impaired in malnutrition cases.
The severity of the impairment is dependent on the degree
of malnutrition in both human and animals. Table 1 contains
a brief description of studies, including 345 malnourished
children and two experimental models that show the impact
of food deprivation on the size of the thymus and the lymphoid
organs [1]. For example, the size of the thymus of 42 malnourished
children was reduced by 90% as compared with a case-match
normal controls. In a second study involving 110 malnourished
children, the thymic area was found to be 20% of the size
in healthy children. In addition, Table 2 contains a brief
description of the result of studies that included 493 malnourished
children who showed impairment in the function of the immune
system; especially the cellular immunity[1].
The reduction in the thymus and the lymphoid
tissue size and the reduction in the function of the immune
system of malnourished children and animals were reversed
after proper feeding as shown in Table 3. For example, the
size of the thymus increased from 20% of normal in a malnourished
child to 107% of normal following 9 weeks of proper feeding.
The reversal of the reduction in CD4+T cell count in HIV+
pregnant women following proper feeding was also reported
by Fawzi et al. [12]. Briefly, the influence of diet on T
cells counts in peripheral blood in 1,075 HIV-infected pregnant
women who had poor nutritional status were studied. The CD4+
T cell counts of the women who received multivitamin increased
from 424/µL to 596/µL during six months of proper feeding
[1,12 ].
The incidence of starvation, parasitic diseases,
septicemia, and low birth weight are very high in Africa and
other developing countries [1,2]. Table 4 contains a brief
description of eleven studies that include the prevalence
of malnutrition and diseases in 1,425 infants and 5,834 children
surveyed in nine countries. For example, the mortality among
299 severely malnourished children in Zambia was 25.8%. Pneumonia
and diarrhea were the major causes of death. In India, 49%
of 183 cases of lymphoadenopathy in children were found to
be due to tuberculosis [1].
High prevalence of malnutrition and disease
in Africa and other developing countries is also reported
by Fauci et al. who stated that, "insufficient consumption
of protein and energy causes loss of both body mass and adipose
tissue, although one or the other loss may predominate in
a given individual. Protein energy malnutrition (PEM) occurs
primarily under two circumstances: in developing nations it
may be present in endemic form, and under famine conditions
the prevalence may approach 25 percent. In children of developing
nations two syndromes of PEM have been distinguished:(1) maramus,
manifested by stunted growth, loss of adipose tissue, generalized
wasting of protein mass; and (2) kwashiorkor, manifested by
growth failure, edema, and hypoalbuminemia, fatty liver, and
preservation of subcutaneous. Mixed forms are common in both
children and adults" [2]
Fauci et al. also stated that "the magnitude
of malnutrition problem worldwide is immense [2]. In 1983
the World Health Organization estimated that 300 million children
had growth retardation secondary to malnutrition. Gastrointestinal
infections frequently precipitate clinical PEM because of
the associated diarrhea, associated anorexia, vomiting, increased
metabolic needs, and decreased intestinal absorption. Parasitic
infections play a major role in many parts of the world. Cell-mediated
immunity is impaired as indicated by all standard tests. Common
infections and opportunistic infections can lead to increased
morbidity and mortality. Pneumonia is common. All wounds and
incisions heal more slowly in PEM. Wound dehiscence is common.
Nearly every aspect of reproduction is impaired in the woman
with PEM, including implantation, fetal growth, lactation,
and parturition. The infants are stunted in size and may have
cognitive impairment if they survive"[2].
Sibanda and Stanczuk reviewed all lymph node
histopathology reports of lymph node biopsy submitted to the
Histopathology unit in Harare, Zimbabwe in the period of January
1988 to June 1990. The commonest diseases in the 2,194 lymph
node specimens submitted were: non specific hyperplasia (33%),
tuberculous lymphadenitis (27%); metastases (12%), Kaposi’s
sarcoma (9%); and lymphomas (7%). Kaposi’s sarcoma involving
the lymph nodes was reported in 176 (9%) of the lymph nodes
[13]. In children, the prevalence was higher in children under
5 years than in 6-15 year bracket. Approximately two thirds
(65%) of all patients with KS were aged between 20 and 40
years [13].
| Table 1. Pathology
of the lymphoid tissues in malnourished children and experimental
animals[1] |
| Study Type |
Population Size |
Description of findings in a population
of 345 children and two experimental animal models |
| Autopsy of Malnur. Children |
118 |
The results of autopsy of malnourished
children showed:
1) Both thymus and peripheral lymphoid tissues are reduced
in bulk in states of protein-calorie malnutrition (PCM),
this reduction being disproportionately greater than the
loss of body weight.
2) Severe thymic atrophy was presented in 70% of marasmus
cases and 85% of Kwashiorkor cases. 59.3% of the children
had marasmic and Kwashiorkor symptoms [14]. |
| |
60 |
The results of autopsy showed:
1) Acute involution and severe chronic atrophy of the
thymus.
2) Atrophy of lymph nodes with depletion of lymphocytes.
3) Atrophy of spleen with depletion of lymphocytes[15].
|
| Clinical Test |
110 |
The mean standardized thymic area (STA)
in severely malnourished children was found to be 20%
of the size in health Children[16]. |
| |
57 |
All severely malnourished children (n=42)
had a severe involution of the thymus gland (average surface
area = 48 mm2). The average size in healthy children is
446 mm2[17]. |
| Animal Studies: Mice |
|
Severely Marasmic mice had extreme atrophy
of the thymus, lymph nodes, spleen and severe lymphocytopenia[1].
|
| Animal Studies: Rats |
|
Growing The status of the thymus of
growing rats fed for 45 days after weaning on a low-quality
dietary protein (7.5% maize) was compared to that in an
age-matched control group receiving a diet containing
casein at the same concentration. Thymus weight, cell
number, and the absolute number of T cells were significantly
lower in experimental group than in the control group[18].
|
| Table 2. Depression
of immune system functions in malnourished children [1]
|
| Study Type |
Population Size |
Description of findings in a population
of 493 children |
| T cells blood number & calorie functions
on in |
22 |
The production of migration inhibitory
factor (MIF) from lymphocytes of children with moderate
protein malnutrition (PCM) was found to be highly impaired
vitro stimulation with Candida albicans antigen[19]. |
| |
33 |
The blood T cells counts and the lymphocyte
response to PHA were found significantly depressed in
14 children suffering from kwashiorkor and 8 children
with marasmus[20]. |
| |
39 |
The lymphocyte transformation rates
in response to PHA stimulation were found to be significantly
lower in 30 children with PCM than 9 healthy control[21].
|
| |
69 |
Significant reduction in the absolute
number and percentage of T-lymphocytes in the blood of
malnourished children were observed[22]. |
| blood |
60 |
Sixty children with malnutrition were
investigated.
1) CD3+ T, CD4+ T, and CD8+ T cells in peripheral blood
of mild malnutrition children were significantly decreased
in contrast to normal control.
2) The reductive degree of CD8+ T and CD4+ T cells correlated
with severity of malnutrition.
3) CD8+ T, CD4+ T and CD4+ T/CD8+ T ratio of moderate
and severe malnutrition with infection were much lower
than those without infection[23]. |
| T and B cells |
100 |
90% of the children were severely malnourished.
1) Significant reduction in the absolute lymphocytes count.
2) Significant reduction in T cells count.
3) Reduction in skin reaction to Dinitrochlorobenzene[24].
|
| B cell Function & Humoral Immunity
|
170 |
The severely malnourished children showed
the following abnormalities compared to normal healthy
group.
1) Significantly higher serum levels IgA1 and IgA2.
2) Reduction in C3 level and an increase in C4 level[25].
|
| Table 3. Recovery
of the lymphoid organs and immune system functions of
malnourished children and experimental animals after feeding
[1] |
| Study Type |
Population Size |
Description of findings in a population
of 150 children and in one experimental model |
| Feeding & Thymus size |
110 |
The thymus size were measured weakly
for 9 weeks in 110 malnourished children, mean age of
16.9 months.
The results show that:
1) The mean standardized thymic are (STA) at week zero
was 70 mm2 (20% of normal), normal STA=350 mm2.
2) The average STA for these children at 5, 7, and 9 weeks
of proper feedings were 63% , 83% , and 107% of normal
respectively[16]. |
| |
40 |
The lymphocyte function of 30 black
children with PCM as assessed by the delayed hypersensitivity
reaction and morphology of lymphocyte transformation was
found to be impaired. Serum cortisol level was elevated.
The function of lymphocyte and cortisol level returned
to normal after 30 days of feeding[23]. |
| Experimental model: Mice |
|
Low protein diets initiated at weaning
in Balb/c mice caused a rapid and profound reduction in
thymus weight and cellularity. Thymus weight fell to less
than that of an involuted thymus of adult mice and remained
depressed for as long as diets were fed. Thymus growth
was reinitiated promptly when high protein diets were
fed to deprived animals. Thymus regeneration appeared
to be due to both a resident population of stem cells[26].
|
| Table 4. List
of selected studies describing the prevalence of malnutrition
and infectious diseases in children in Africa and other
developing nations[1] |
| Parameters Studied |
Country |
Results of studies in a population of
1425 infants and 5834 children |
| Birth weights |
Nigeria |
18.7% of 1041 pregnant women delivered
low birth weight babies <2.5 kg[27]. |
| |
Kenya |
11% of 123 pregnant women delivered
low birth weight babies[28]. |
| Nutritional Status & health in Children
|
Trinidad & Tobago |
49.5% of 1620 children evaluated were
suffering from some degree of malnutrition and 12.5% were
considered as moderately or severely malnourished[29].
|
| |
Uganda |
21.5% of 261 infants and toddles examined
were found in poor health (3.8% suffering from kwashiorkor
and 5.7 with marasmus).
Infections rate: 23% diarrhea, 32% malaria[30] |
| |
Nigeria |
Prevalence of malnutrition was determined
in 204 children (3-5y): was 60.8% for stunting, 7.4% for
wasting, and for 27.5% underweight[31]. |
| |
Congo |
The health status of 2429 children were
evaluated. Prevalence was 27.5% for stunting & 5.5%
for Wasting = 5.5%[32]. |
| Goiter |
Lesotho Highlands |
17.5% of 10-14 years old children had
goiter (Children from 395 households were evaluated)[33].
|
| Septicemia |
Nigeria |
The incidence of septicemia was 9.6%
of medical admissions and the overall mortality rate =
28.3%[34]. |
| Tuberculosis |
India |
49% of 183 cases of lympadenopathy in
children was found to be tuberculosis[3]. |
| Parasitic infection |
Nigeria |
704 children (5-19 years) were evaluated.
Infection rates: 32.4% hookworm; 22.9% ascariasis; 17%
hematuria (schistomiasis)[35]. |
| Mortality Rate |
Zambia |
The mortality rate among 299 severely
malnourished children was 25.8%. Pneumonia and diarrhea
were the major causes of death[36]. |
Mohammed A. Al-Bayati, PhD, DABT, DABVT.
Toxi-Health International
Dixon, CA 95620
http://www.toxi-health.com
Email:maalbayati@toxi-health.com
Phone: (707) 678-4484
Fax: (707) 678-8505
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|